Legume and isoflavone intake and prostate cancer risk: The Multiethnic Cohort Study

Findings from studies of legume, soy and isoflavone intake and prostate cancer risk are as yet inconclusive, although soy has received considerable attention due to its high phytoestrogen content. Therefore, the present study investigated the relationship of these dietary exposures to prostate cancer risk in the Multiethnic Cohort Study in Hawaii and Los Angeles. The analyses included 82,483 men who completed a detailed quantitative food frequency questionnaire in 1993-1996. A total of 4,404 prostate cancer cases including 1,278 nonlocalized or high-grade cases were recorded during the average follow-up period of 8 years. Multivariate relative risks (RR) and 95% of confidence intervals (CI) were estimated using Cox proportional hazards models with age as the time metric. Among men with the highest intake of legumes, the risk reduction was 11% for total prostate cancer (RR = 0.89, 95% CI = 0.80-0.99, p for trend = 0.007) and 26% for nonlocalized or high-grade cancer (RR = 0.74, 95% CI = 0.61-0.90, p for trend = 0.007) compared to men with the lowest intake. Similar risk reductions were observed for soy products and for legumes excluding soy products in separate analyses. We found no significant risk reduction associated with intake of total or specific isoflavones for either total prostate cancer or for nonlocalized or high-grade cancer. The findings of our study suggest that legume intake is associated with a moderate reduction in prostate cancer risk and that the isoflavones in soy products are probably not responsible for this effect.     

A prospective study on intake of animal products and risk of prostate cancer

Objective: Association between animal products and prostate cancer have been observed in numerous observational studies, but it is not clear whether the high fat content of these foods or some other component accounts for these associations. We examine these associations among 51,529 men who contributed detailed dietary data. Methods: Participants of the Health Professionals Follow-Up Study completed a semiquantitative food-frequency questionnaire in 1986, and subsequently in 1990 and 1994. Other data on potential risk factors were collected at baseline and in subsequent questionnaires during follow-up. Between 1986 and 1996, 1897 total cases of prostate cancer (excluding stage A₁) and 249 metastatic cancers were identified. We used pooled logistic regression for analyses of diet and prostate cancer. Results: Intakes of total meat, red meat, and dairy products were not associated with risk of total or advanced prostate cancer. An elevated risk for metastatic prostate cancer was observed with intake of red meat (relative risk (RR) = 1.6 for top vs. bottom quintile comparison, 95% confidence interval (CI) = 1.0–2.5); this association was slightly attenuated after controlling for saturated and -linolenic fatty acids (RR = 1.5, 95% CI = 0.88–2.5). Processed meats, bacon and beef, pork or lamb as a main dish each contributed to an elevated risk of metastatic prostate cancer. Dairy product intake increased risk of metastatic prostate cancer (RR = 1.4, 95% CI = 0.91–2.2 for top vs. bottom quintile comparison), but no association remained after controlling for calcium and other fatty acids. A high intake in both red meat and dairy product was associated with a statistically significant two-fold elevation in risk of metastatic prostate cancer, compared to low intake of both products; however, most of the excess risk could be explained by known nutritional components of these foods. Conclusions: Intakes of red meat and dairy products appear to be related to increased risk of metastatic prostate cancer. While known nutrients, such as calcium and fatty acids, may explain most of the dairy association observed, it appears that a portion of the risk of metastatic prostate cancer associated with red meat intake remains unexplained.     

Association between ambient air pollution and breast cancer risk: The multiethnic cohort study

Previous studies using different exposure methods to assess air pollution and breast cancer risk among primarily whites have been inconclusive. Air pollutant exposures of particulate matter and oxides of nitrogen were estimated by kriging (NO_x, NO₂, PM₁₀, PM_2.5), land use regression (LUR, NO_x, NO₂) and California Line Source Dispersion model (CALINE4, NO_x, PM_2.5) for 57,589 females from the Multiethnic Cohort, residing largely in Los Angeles County from recruitment (1993–1996) through 2010. Cox proportional hazards models were used to examine the associations between time-varying air pollution and breast cancer incidence adjusting for confounding factors. Stratified analyses were conducted by race/ethnicity and distance to major roads. Among all women, breast cancer risk was positively but not significantly associated with NO_x (per 50 parts per billion [ppb]) and NO₂ (per 20 ppb) determined by kriging and LUR and with PM_2.5 and PM₁₀ (per 10 μg/m³) determined by kriging. However, among women who lived within 500 m of major roads, significantly increased risks were observed with NO_x (hazard ratio [HR] = 1.35, 95% confidence interval [95% CI]: 1.02–1.79), NO₂ (HR = 1.44, 95% CI: 1.04–1.99), PM₁₀ (HR = 1.29, 95% CI: 1.07–1.55) and PM_2.5 (HR = 1.85, 95% CI: 1.15–2.99) determined by kriging and NO_x (HR = 1.21, 95% CI:1.01–1.45) and NO₂ (HR = 1.26, 95% CI: 1.00–1.59) determined by LUR. No overall associations were observed with exposures assessed by CALINE4. Subgroup analyses suggested stronger associations of NO_x and NO₂ among African Americans and Japanese Americans. Further studies of multiethnic populations to confirm the effects of air pollution, particularly near-roadway exposures, on the risk of breast cancer is warranted.     

Red and processed meat intake and cancer risk: Results from the prospective NutriNet‐Santé cohort study

The International Agency for Research on Cancer (WHO‐IARC) classified red meat and processed meat as probably carcinogenic and carcinogenic for humans, respectively. These conclusions were mainly based on studies concerning colorectal cancer, but scientific evidence is still limited for other cancer locations. In this study, we investigated the prospective associations between red and processed meat intakes and overall, breast, and prostate cancer risk. This prospective study included 61,476 men and women of the French NutriNet‐Santé cohort (2009–2015) aged ≥35 y and who completed at least three 24 hrs dietary records during the first year of follow‐up. The risk of developing cancer was compared across sex‐specific quintiles of red and processed meat intakes by multivariable Cox models. 1,609 first primary incident cancer cases were diagnosed during follow‐up, among which 544 breast cancers and 222 prostate cancers. Red meat intake was associated with increased risk of overall cancers [HR_Q5vs.Q1=1.31 (1.10–1.55), p_trend = 0.01) and breast cancer (HR_Q5vs.Q1 = 1.83 (1.33–2.51), p_trend = 0.002]. The latter association was observed in both premenopausal [HR_Q5vs.Q1=2.04 (1.03–4.06)] and postmenopausal women [HR_Q5vs.Q1=1.79 (1.26‐2.55)]. No association was observed between red meat intake and prostate cancer risk. Processed meat intake was relatively low in this study (cut‐offs for the 5th quintile = 46 g/d in men and 29 g/d in women) and was not associated with overall, breast or prostate cancer risk. This large cohort study suggested that red meat may be involved carcinogenesis at several cancer locations (other than colon‐rectum), in particular breast cancer. These results are consistent with mechanistic evidence from experimental studies.     

Estimated phytanic acid intake and prostate cancer risk: a prospective cohort study

Phytanic acid is a saturated fatty acid found predominantly in red meat and dairy products and may contribute to increases in prostate cancer risk that are observed with higher intakes of these foods. We constructed a novel summary measure of phytanic acid intake and prospectively examined its association with prostate cancer risk in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study--a cohort of Finnish male smokers aged 50-69 years. Diet was assessed at baseline in 27,111 participants using a validated 276-item dietary questionnaire. Since phytanic acid is not currently included in food composition tables, we used the published phytanic acid content of 151 major food items to estimate total daily intake. During up to 21 years of follow-up, a total of 1,929 incident prostate cancer cases (including 438 advanced cases) were identified. Higher phytanic acid intake, though unrelated to the risk of localized disease [relative risks (RR) and 95% confidence intervals (CI) for increasing quartiles of intake = 1.00 (ref), 0.83 (0.68-1.01), 0.76 (0.62-0.94) and 0.91 (0.74-1.13); p trend = 0.23], was associated with increased risks of advanced prostate cancer [RR and 95% CI = 1.00 (ref), 1.43 (1.09-1.89), 1.31 (0.99-1.75) and 1.38 (1.02-1.89); p trend = 0.06]. This association appeared to be driven predominantly by phytanic acid obtained from dairy products (particularly butter). Our study indicates that phytanic acid may contribute to previously observed associations between high-fat animal foods (particularly dairy products) and prostate cancer risk, although some caution is warranted as it may be acting as a surrogate marker of dairy fat.     

Alcohol consumption and prostate cancer risk: results from the Melbourne collaborative cohort study

Although there is little evidence to support an association between alcohol consumption and prostate cancer risk, questions remain concerning the effect on aggressive and nonaggressive tumours and the pattern and type of alcohol consumed. In a prospective cohort of 16,872 men aged 27-70 years at recruitment and followed-up from 1994 to the end of 2003, 732 incident prostate cancers were identified through the local population cancer registry, including 132 aggressive cases and 53 prostate cancer deaths. Detailed information on alcohol consumption was taken at baseline by trained interviewers using a structured questionnaire. Overall, alcohol intake was not associated with prostate cancer incidence. Compared to abstainers, men consuming 1-19 g/d of alcohol had a slightly reduced incidence of aggressive prostate cancers (hazard ratio 0.67; 95% confidence interval (CI) 0.43, 1.06) and prostate cancer mortality (hazard ratio 0.56; 95% CI 0.28, 1.14), but their risk of nonaggressive prostate cancers was close to unity (hazard ratio 1.09; 95% CI 0.85, 1.40). No significant association with pattern of drinking or type of alcoholic beverage was found. Our results show that alcohol consumption does not influence overall prostate cancer incidence but we found suggestive evidence that alcohol consumption might decrease the incidence of aggressive prostate cancer and mortality.     

A prospective cohort study of red wine consumption and risk of prostate cancer

In light of recent, strong inverse findings between lifetime red wine consumption and prostate cancer among younger men, we revisited our previous cohort analysis to more thoroughly investigate red wine consumption and prostate cancer in the Health Professionals Follow-up Study (HPFS). In 1986, HPFS participants reported their average consumption of red wine, white wine, beer and liquor during the past year, and their change in alcohol consumption over the prior 10 years. Prostate cancer diagnoses were ascertained on each biennial questionnaire and confirmed by medical record review. Between 1986 and 2002, 3,348 cases of prostate cancer were diagnosed among 45,433 eligible participants. Using men who did not consume red wine as the reference, no linear trend was observed between red wine consumption and prostate cancer in the full analytic cohort (p-trend = 0.57). Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed 4 glasses/week, resulting in a lack of linear trend. These findings suggest that red wine does not contribute appreciably to the etiology of prostate cancer.     

Meat and fat intake and pancreatic cancer risk in the Netherlands Cohort Study

Meat contains numerous carcinogens, such as heterocyclic amines, polycyclic aromatic hydrocarbons, and N‐nitroso compounds, which can be derived either from natural food or during the process of food preparation. These carcinogens may increase pancreatic cancer risk. Furthermore, studies in animals showed that polyunsaturated fatty acids, especially linoleic acid, increase pancreatic cancer risk. We examined prospectively the relation between pancreatic cancer risk and intake of fresh meat, processed meat, fish, eggs, total fat, and different types of fat. The Netherlands Cohort Study consisted of 120,852 men and women who completed a baseline questionnaire in 1986. After 13.3 years of follow‐up, 350 pancreatic cancer cases (66% microscopically confirmed) were available for analysis. A validated 150‐item food‐frequency questionnaire was used to calculate intake of fresh meat, processed meat, fish, eggs, fat and different types of fat. No association was found when examining the association between intake of fresh meat, other types of meat, fish, eggs, dietary intake of total fat and different types of fat and risk of pancreatic cancer. It is important for future studies to investigate the relation between different meat‐cooking methods and pancreatic cancer. © 2009 UICC     

Use of terbinafine and risk of death in patients with prostate cancer: A population-based cohort study

Terbinafine is used for the treatment of several superficial fungal infections. In silico analyses and animal models suggest that terbinafine might have an anti-tumor effect. We aimed to explore whether subsequent administration of terbinafine might be associated with a lower mortality rate in patients with prostate cancer. We identified patients diagnosed with prostate cancer between July 2005 and December 2014 from the Swedish Cancer Registry, and linked them to the Swedish Prescribed Drug Register to ascertain subsequent use of terbinafine. A total of 799 patients received oral treatment of terbinafine during the study period with a mortality rate of 18.6 per 1,000 person-years. Compared to patients who did not use terbinafine and adjusting for a range of confounding factors, patients that received oral treatment of terbinafine had a decreased risk of death from prostate cancer (HR, 0.53; 95% CI, 0.38–0.73) and a decreased risk of death overall (HR, 0.64; 95% CI, 0.52–0.77). To account for indication bias, we further identified 907 patients who received topical use of terbinafine. However, the risk of death from prostate cancer in patients with topical use of terbinafine was 0.92 (95% CI 0.74–1.12) and the risk of death overall was 1.03 (95% CI 0.91–1.17) as compared to the controls, which suggests that there was no association between risk of death in patients with prostate cancer with topical use of terbinafine. These findings suggest that this drug's potential anti-tumor effect needs to be explored further.     

Body size,adult BMI gain and endometrial cancer risk: the multiethnic cohort

The effect of body size and change in BMI on endometrial cancer risk across different racial/ethnic groups has not been studied. We examined the association between body size and endometrial cancer risk and potential effect modification of other risk factors among 50,376 women in the Multiethnic Cohort Study. During 10.3 years of follow‐up, 463 endometrial cancer cases were identified. Epidemiologic data were collected from the baseline questionnaire. “BMI change” was defined as the percentage of body mass index change from age 21 to the time of recruitment. Women who were heavier at age 21 or at baseline (weight ≥ 53.5 kg or ≥ 63.9 kg, respectively) had an increased endometrial cancer risk compared to the lowest quartile of weight during the respective periods. BMI gain ≥ 35% had a RR of 4.12 (95% CI: 2.69, 6.30) compared to the reference group (−5% ≤ BMI change <+5%). Women who averaged an annual BMI gain ≥ 1% had a >3.21‐fold (95% CI: 2.37, 4.33) increased risk compared to women who maintained a stable adult BMI (−0.25 to <+0.25%). The highest risk associated with BMI gain was observed among nulliparous women and postmenopausal women who never used hormone therapy. Although African Americans and Whites showed an increase in risk after ≥35% BMI gain, Japanese Americans showed an increase in risk with much smaller gain (≥5%). In conclusion, adult obesity and increase in adiposity are risk factors for endometrial cancer; and the risk associated with these factors may vary across racial/ethnic groups.     

Meat intake,cooking methods and risk of proximal colon,distal colon and rectal cancer: The Norwegian Women and Cancer (NOWAC) cohort study

Red and processed meat intake is an established risk factor for colorectal cancer (CRC), but epidemiological evidence by subsite and sex is still limited. In the population‐based Norwegian Women and Cancer cohort, we examined associations of meat intake with incident proximal colon, distal colon and rectal cancer, in 84,538 women who completed a validated food frequency questionnaire (FFQ) during 1996–1998 or 2003–2005 (baseline or exposure update) at age 41–70 years, with follow‐up by register linkages through 2009. We also examined the effect of meat cooking methods in a subsample (n = 43,636). Multivariable hazard ratios (HRs) were estimated by Cox regression. There were 459 colon (242 proximal and 167 distal), and 215 rectal cancer cases with follow‐up ≥ 1 (median 11.1) year. Processed meat intake ≥60 vs. <15 g/day was associated with significantly increased cancer risk in all subsites with HRs (95% confidence interval, CI) of 1.69 (1.05–2.72) for proximal colon, 2.13 (1.18–3.83) for distal colon and 1.71 (1.02–2.85) for rectal cancer. Regression calibration of continuous effects based on repeated 24‐hr dietary recalls, indicated attenuation due to measurement errors in FFQ data, but corrected HRs were not statistically significant due to wider CIs. Our study did not support an association between CRC risk and intake of red meat, chicken, or meat cooking methods, but a high processed meat intake was associated with increased risk of proximal colon, distal colon and rectal cancer. The effect of processed meat was mainly driven by the intake of sausages.     

Dietary fat intake and liver cancer risk: A prospective cohort study in Chinese women

Objective:This study aimed to determine whether dietary fat intake increased liver cancer risk in Chinese women from a prospective population-based cohort.Methods:A total of 72,704 Chinese women were followed up from the time of baseline recruitment (1996–2000) to the end of 2016. Dietary fat intake was calculated using a validated food frequency questionnaire. The Cox regression model was used to assess the hazard ratio (HR) and 95% confidence intervals (CI) for dietary fat intake and liver cancer risk.Results:We identified 252 incident liver cancer cases out of 1,267,845 person-years during the overall follow-up time. Null associations, neither in quartiles nor per standard deviation (SD) increment, were detected between liver cancer risk and dietary total fat, fat subtypes and subtype ratios, and food sources. The HR (95% CI) of the 1-SD increment was 1.03 (0.90–1.17) for total fat, 1.06 (0.93–1.20) for saturated fat, 1.06 (0.93–1.21) for monounsaturated fat, and 1.00 (0.89–1.13) for polyunsaturated fat. Similar null associations were observed in stratification analyses according to body mass index and menopausal status.Conclusions:In our prospective cohort study, no significant association was observed in Chinese women between dietary fat and liver cancer risk, and in stratification and sensitivity analyses.     

Salt intake,cured meat consumption,refrigerator use and stomach cancer incidence: a prospective cohort study (Netherlands)

Objective: Many case–control studies have reported that salt and cured meat intake are positively, and refrigerator use is inversely, associated with stomach cancer risk. In the current prospective study these associations were evaluated. Methods: The Netherlands Cohort Study consisted of 120,852 men and women ages 55–69 years at baseline in 1986. Salt exposure was measured by calculating mean daily sodium intake (dietary salt) from 150 food items and by specific salt questions. After 6.3 years of follow-up, 282 incident stomach cancer cases were available for analyses. Case-cohort analyses were based on the 282 cases and 3123 subcohort members. Results: In multivariate analyses adjusted for age, sex, smoking, education, stomach disorders, history of stomach cancer in the family, rate ratios (RR) for increasing quintiles of energy-adjusted intake of dietary salt were 1.00, 1.49, 1.03, 1.54 and 1.18, respectively (p trend = 0.43). An inverse association was found between stomach cancer and salt added at the hot meal (p trend = 0.04). For salt added to home-made soup, use of salt at the table, salt preference and duration of refrigerator use, no associations were observed. Positive associations were found for bacon (RR highest/lowest intake = 1.33; 95% CI = 1.03–1.71) and other sliced cold meat (RR highest/lowest intake = 1.29; 95% CI = 0.96–1.72), but not for smoked sausage, total cold meats, rashers/bacon, boiled ham and smoked beef/pork loin roll. Separate analyses among subjects with self-reported stomach disorders revealed higher RR of stomach cancer for dietary salt and several types of cured meat. Conclusion: The present findings suggest that intake of dietary salt and several types of cured meat were weakly positively associated with stomach cancer risk.     

Pulmonary tuberculosis increases the risk of lung cancer: a population-based cohort study

BACKGROUND:

The possible effect of pulmonary tuberculosis (TB) on subsequent lung cancer development has been suspected, but the evidence remains inconsistent. The purpose of this study was to perform a nationwide population‐based cohort study to investigate the risk of lung cancer after pulmonary TB infection.

METHODS:

This nationwide population‐based cohort study was based on data obtained from the Taiwan National Health Insurance Database. In total, 5657 TB patients and 23,984 controls matched for age and sex were recruited for the study from 1997 to 2008.

RESULTS:

The incidence rate of lung cancer (269 of 100,000 person‐years) was significantly higher in the pulmonary TB patients than that in controls (153 of 100,000 person‐years) (incidence rate ratio [IRR], 1.76; 95% confidence interval [CI], 1.33‐2.32; P < .001). Compared with the controls, the IRRs of lung cancer in the TB cohort were 1.98 at 2 to 4 years, 1.42 at 5 to 7 years, and 1.59 at 8 to 12 years after TB infections. The multivariate Cox proportional hazards model revealed pulmonary TB infections (hazard ratio [HR], 1.64; 95% CI, 1.24‐2.15; P < .001) and chronic obstructive pulmonary disease (HR, 1.09; 95% CI, 1.03‐1.14; P = .002) to be independent risk factors for lung cancer.

CONCLUSIONS:

Pulmonary infection with TB is associated with an increased risk of lung cancer. Cancer 2011. © 2010 American Cancer Society.     

Sugar intake and colorectal cancer risk: A prospective Japanese cohort study

The influence of sugar consumption on the risk of colorectal cancer (CRC) remains controversial. Prospective cohort studies focusing on total and specific types of sugar intake among the Asian population who have different patterns of sugar intake sources than American and European populations are scarce. We intended to examine the association of sugar intake with CRC risk among middle-aged adults in a Japanese large-scale population-based cohort study. The participants (42,405 men and 48,600 women) who were 45–74 years old and answered the questionnaire in 1995–1999 in the Japan Public Health Center-based Prospective Study were followed up until December 2013. Total sugars, total fructose, and specific types of sugar intake were estimated using a validated 147-item food frequency questionnaire and divided into quintiles (Q1–Q5). We used Cox proportional hazard regression models adjusted for potential confounders to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During the follow-up, 2118 CRC cases (1226 men and 892 women) were identified. We did not observe any clear association between all types of sugar intake and an increased risk of CRC. Analyses by tumor sites yielded a positive association of total sugar consumption with rectal cancer in women (1.75 [1.07–2.87] for Q1 vs. Q5; p _{linear trend} = 0.03), but no statistically significant trend was detected among men. Sugar intake was not associated with CRC risk in middle-aged Japanese adults. However, for rectal cancer, the probability of an increased risk among women with a higher total sugar intake cannot be excluded.     

Relationship between vegetable and carotene intake and risk of prostate cancer: the JACC study

Background:

We examined the associations of intakes of vegetables and carotenes with risk of prostate cancer in Japanese.

Methods:

A total of 15 471 Japanese men participating in the Japan Collaborative Cohort study completed a questionnaire including food intake. Of them, 143 incident prostate cancers were documented. We examined the associations stated above by using Cox proportional hazard model.

Results:

Vegetable intake was not associated with the risk of prostate cancer, but so was dietary alpha-carotene intake. The multivariable hazard ratio (95%CI) in the secondary highest and highest quintiles of alpha-carotene intake was 0.50 (0.26–0.98) (P=0.043) and 0.46 (0.22–0.97) (P=0.041) (P for trend=0.224), respectively. Beta-carotene intake was not associated with the risk of prostate cancer.

Conclusion:

Alpha-carotene intake was associated with lower risk of prostate cancer among Japanese.     

Alcohol consumption and endometrial cancer risk: the multiethnic cohort

The role of alcohol intake in the etiology of endometrial cancer is unclear. We examined the impact of alcohol intake on endometrial cancer risk among 41,574 postmenopausal African-American, Japanese-American, Latina, Native-Hawaiian and White women recruited to the prospective Multiethnic Cohort Study in 1993-1996. During an average of 8.3 years of follow-up, 324 incident invasive endometrial cancer cases were identified among these women. Data on alcohol intake and endometrial cancer risk factors were obtained from the baseline questionnaire. Relative risks (RRs) and 95% confidence intervals (CIs) for endometrial cancer associated with alcohol intake were estimated using log-linear (Cox) proportional hazard models stratified by age, year of recruitment, ethnicity and study center, and adjusted for several confounding factors. Increased alcohol consumption was associated with increased risk (p trend = 0.013). Compared to nondrinkers, women consuming >or=2 drinks/day had a multivariate RR of 2.01 (95% CI: 1.30, 3.11). There was no increase in risk associated with <1 drink/day (RR = 1.01; 95% CI: 0.77, 1.33) and 1 to <2 drinks/day (RR = 1.09; 95% CI: 0.62, 1.93). There was no clear effect modification by body mass index, postmenopausal hormone use, parity, oral contraceptive use or smoking status, though our power to detect such interactions was limited. Our results suggest that only alcohol consumption equivalent to 2 or more drinks per day increases risk of endometrial cancer in postmenopausal women.     

Associations between unprocessed red and processed meat,poultry, seafood and egg intake and the risk of prostate cancer: A pooled analysis of 15 prospective cohort studies

Reports relating meat intake to prostate cancer risk are inconsistent. Associations between these dietary factors and prostate cancer were examined in a consortium of 15 cohort studies. During follow‐up, 52,683 incident prostate cancer cases, including 4,924 advanced cases, were identified among 842,149 men. Cox proportional hazard models were used to calculate study‐specific relative risks (RR) and then pooled using random effects models. Results do not support a substantial effect of total red, unprocessed red and processed meat for all prostate cancer outcomes, except for a modest positive association for tumors identified as advanced stage at diagnosis (advanced(r)). For seafood, no substantial effect was observed for prostate cancer regardless of stage or grade. Poultry intake was inversely associated with risk of advanced and fatal cancers (pooled multivariable RR [MVRR], 95% confidence interval, comparing ≥45 vs. <5 g/day: advanced 0.83, 0.70–0.99; trend test p value 0.29), fatal, 0.69, 0.59–0.82, trend test p value 0.16). Participants who ate ≥25 versus <5 g/day of eggs (1 egg ～ 50 g) had a significant 14% increased risk of advanced and fatal cancers (advanced 1.14, 1.01–1.28, trend test p value 0.01; fatal 1.14, 1.00–1.30, trend test p value 0.01). When associations were analyzed separately by geographical region (North America vs. other continents), positive associations between unprocessed red meat and egg intake, and inverse associations between poultry intake and advanced, advanced(r) and fatal cancers were limited to North American studies. However, differences were only statistically significant for eggs. Observed differences in associations by geographical region warrant further investigation.     

A prospective cohort study of physical activity and body size in relation to prostate cancer risk (United States)

Objectives: To examine the associations of physical activity and body size with risk of prostate cancer. Methods: At baseline in 1988, 8922 men (mean age 67 years) completed a health questionnaire which included information on physical activity, body weight, and waist girth. In a subgroup (74% of men), physical activity data also had been provided in 1962 or 1966 and again in 1977. Additionally, body weight measured at age 18 was available for 92% of men. During follow-up from 1988 through 1993, 439 men developed prostate cancer. Results: In multivariate analyses that accounted for potential confounders, the RRs (95% CI) for <4200, 4200–8399, 8400–12,599, and 12,600 kJ/week of physical activity at baseline were 1.00 (referent), 1.13 (0.84–1.52), 0.96 (0.68–1.35), and 1.04 (0.79–1.38), respectively. For body mass indexes (BMI) of <22.5, 22.5–24.9, 25.0–27.4, and 27.5 kg/m² at baseline, corresponding results were 1.00 (referent), 1.27 (0.94–1.71), 1.26 (0.92–1.72), and 1.02 (0.68–1.53), respectively. For waist girths of 86.4, 86.5–91.4, 91.5–96.5, and >96.5 cm, they were 1.00 (referent), 1.30 (0.96–1.76), 1.31 (0.96–1.80), and 1.19 (0.85–1.65), respectively. Combining physical activity measures from the past, or examining vigorous activities only, did not yield any significant associations. BMI at age 18 also was not related to risk. Conclusion: These findings do not support a role of physical activity or body weight in prostate cancer etiology.     

Acne and risk of prostate cancer

In a recent study, prostatectomy specimens from which Propionibacterium acnes was cultured were more likely to have inflammation than culture-negative specimens or specimens positive for other bacteria, leading the authors to hypothesize that P. acnes-mediated inflammation may contribute to prostate carcinogenesis. To indirectly explore associations between P. acnes and prostate cancer, we investigated severe acne, as measured by tetracycline use for 4 or more years, in relation to incident prostate cancer in the Health Professionals Follow-up Study. On the 1992 follow-up questionnaire, participants were asked whether they had ever used "tetracycline for at least 2 months at a time (e.g., for acne or other reason)" and their duration of use. Prostate cancer diagnoses were ascertained on each subsequent biennial questionnaire and confirmed by medical record review. Between 1992 and 2002, 2,147 cases of prostate cancer were reported among 34,629 eligible participants. Men who used tetracycline for 4 or more years had a significantly higher risk of prostate cancer (16 cases, 1,569 person-years) than men who did not use tetracycline (2,071 cases, 304,822 person-years, multivariable-adjusted RR = 1.70, 95% CI: 1.03-2.80). Although intriguing, this finding should be viewed cautiously because of the small number of exposed cases, indirect assessment of severe acne, and complex etiology of acne, which is not limited to P. acnes infection. Therefore, additional biologic and epidemiologic studies are necessary to determine and elucidate the possible role of P. acnes infection in prostate carcinogenesis.