***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: IMPORTANCE 5α-Reductase inhibitors ( 5ARIs ) are widely used for benign prostatic hyperplasia despite controversy regarding potential risk of high- grade prostate cancer with use . Furthermore , the effect of 5ARIs on progression and prostate cancer death remains unclear . OBJECTIVE To determine the association between 5ARI use and development of high- grade or lethal prostate cancer . DESIGN , SETTING , AND PARTICIPANTS Prospect i ve observational study of 38,058 men followed up for prostate cancer diagnosis and outcomes between 1996 and 2010 in the Health Professionals Follow-up Study . EXPOSURES Use of 5ARIs between 1996 and 2010 . MAIN OUTCOMES AND MEASURES Cox proportional hazards models were used to estimate risk of prostate cancer diagnosis or development of lethal disease with 5ARI use , adjusting for possible confounders including prostate specific antigen testing . RESULTS During 448,803 person-years of follow-up , we ascertained 3681 incident prostate cancer cases . Of these , 289 were lethal ( metastatic or fatal ) , 456 were high grade ( Gleason sum [ GS ] 8 - 10 ) , 1238 were GS 7 , and 1600 were low grade ( GS 2 - 6 ) . A total of 2878 ( 7.6 % ) men reported use of 5ARIs between 1996 and 2010 . After adjusting for confounders , men who reported ever using 5ARIs over the study period had a reduced risk of overall prostate cancer ( hazard ratio [ HR ] , 0.77 ; 95 % CI , 0.65 - 0.91 ) . 5ARI users had a reduced risk of GS 7 ( HR , 0.67 ; 95 % CI , 0.49 - 0.91 ) and low- grade ( GS 2 - 6 ) prostate cancer ( HR , 0.74 ; 95 % CI , 0.57 - 0.95 ) . 5ARI use was not associated with risk of high- grade ( GS 8 - 10 ) prostate cancer ( HR , 0.97 ; 95 % CI , 0.64 - 1.46 ) or lethal disease ( HR , 0.99 ; 95 % CI , 0.58 - 1.69 ) . Increased duration of use was associated with significantly lower risk of overall prostate cancer ( HR for 1 year of additional use , 0.95 ; 95 % CI , 0.92 - 0.99 ) , localized ( HR , 0.95 ; 95 % CI , 0.90 - 1.00 ) , and low- grade disease ( HR , 0.92 ; 95 % CI , 0.85 - 0.99 ) . There was no association for lethal , high- grade , or grade 7 disease . CONCLUSIONS AND RELEVANCE While 5ARI use was not associated with developing high- grade or lethal prostate cancer , it was associated with a reduction in low- grade , GS 7 , and overall prostate cancer . Because the number of patients with high- grade or lethal prostate cancer in our cohort was limited , we can not rule out potential risk of harm with 5ARI use BACKGROUND Fish and seafood n-3 fatty acids may prevent or delay the progression of prostate cancer , but epidemiologic studies do not uniformly support this hypothesis . OBJECTIVE We examined the relation of fish and seafood n-3 fatty acid intakes with  prostate cancer incidence and mortality . DESIGN We conducted a prospect i ve cohort study among 20,167 men participating in the Physician 's Health Study who were free of cancer in 1983 . RESULTS During 382 144 person-years of follow-up , 2161 men were diagnosed with prostate cancer and 230 died of prostate cancer . Fish intake was unrelated to prostate cancer incidence . Survival analysis among the men diagnosed with prostate cancer revealed that those consuming fish > or=5 times/wk had a 48 % lower risk of prostate cancer death than did men consuming fish less than once weekly [ relative risk ( RR ) = 0.52 ; 95 % CI : 0.30 , 0.91 ; P for trend = 0.05 ] . A similar association was found between seafood n-3 fatty acid intake and prostate cancer mortality ( RR(Q5 versus Q1 ) = 0.64 ; 95 % CI : 0.42 , 0.99 ; P for trend = 0.02 ) . These associations became stronger when the analyses were restricted to clinical ly detected cases . CONCLUSION These results suggest that fish intake is unrelated to prostate cancer incidence but may improve prostate cancer survival BACKGROUND Laboratory studies have shown that n-3 fatty acids inhibit and n-6 fatty acids stimulate prostate tumor growth , but whether the dietary intake of these fatty acids affects prostate cancer risk in humans remains unclear . OBJECTIVE We prospect ively evaluated the association between intakes of alpha-linolenic ( ALA ; 18:3n-3 ) , eicosapentaenoic ( EPA ; 20:5n-3 ) , docosahexaenoic ( DHA ; 22:6n-3 ) , linoleic ( LA ; 18:2n-6 ) , and arachidonic ( AA ; 20:4n-6 ) acids and prostate cancer risk . DESIGN A cohort of 47 866 US men aged 40 - 75 y with no cancer history in 1986 was followed for 14 y. RESULTS During follow-up , 2965 new cases of total prostate cancer were ascertained , 448 of which were advanced prostate cancer . ALA intake was unrelated to the risk of total prostate cancer . In contrast , the multivariate relative risks ( RRs ) of advanced prostate cancer from comparisons of extreme quintiles of ALA from nonanimal sources and ALA from meat and dairy sources were 2.02 ( 95 % CI : 1.35 , 3.03 ) and 1.53 ( 0.88 , 2.66 ) , respectively .  EPA and DHA intakes were related to lower prostate cancer risk . The multivariate RRs of total and advanced prostate cancer from comparisons of extreme quintiles of the combination of EPA and DHA were 0.89 ( 0.77 , 1.04 ) and 0.74 ( 0.49 , 1.08 ) , respectively . LA and AA intakes were unrelated to the risk of prostate cancer . The multivariate RR of advanced prostate cancer from a comparison of extreme quintiles of the ratio of LA to ALA was 0.62 ( 0.45 , 0.86 ) . CONCLUSIONS Increased dietary intakes of ALA may increase the risk of advanced prostate cancer . In contrast , EPA and DHA intakes may reduce the risk of total and advanced prostate cancer Purpose A few recent epidemiological observations suggest that anticoagulant medications may protect against  prostate cancer development . Most studies have been small or subjected to method ological issues , including potential confounding . We provide here new evidence on this association in the context of a population -based case – control study of prostate cancer conducted in Montreal , Canada . Methods Cases were 1,588 men with incident prostate cancer , aged ≤75 years , diagnosed across French hospitals in the Montreal area between 2005 and 2009 . Concurrently , 1,618 population controls from the same residential area and age distribution ( ±5 years ) were r and omly selected from the electoral list of French-speaking men .  In-person interviews elicited information on socio-demographic , lifestyle and environmental factors , along with a detailed medical history . Unconditional logistic regression was used to assess the association between lifetime use  of anticoagulants  and prostate cancer risk . Results 102 subjects ( 2.6 % of cases and 3.7 % of controls ) reported a history  of oral anticoagulant therapy . After controlling for age , ancestry , education , family history of prostate cancer , prostate cancer screening frequency , diabetes , body mass index and statin use , ever use of oral anticoagulants showed a weak inverse , non-statistically significant association with prostate cancer ( odds ratio 0.76 , 95 % confidence interval 0.50–1.16 ) . Similar results were observed in analyses considering duration of use or indication for use , restricted to subjects recently screened or stratified by cancer aggressiveness . Conclusions Our findings provide weak support for a protective effect of oral anticoagulant therapy against prostate cancer . Further confirmation is required , especially in light of potential bleeding complications associated with anticoagulants PURPOSE A r and omized , placebo controlled clinical trial of folic acid supplementation for the chemoprevention of colorectal adenoma revealed an increased incidence of prostate cancer in the treatment group . Limited data exist on postdiagnostic folate/folic acid intake and the risk of prostate cancer progression . We prospect ively examined the association between postdiagnostic folate consumption and the risk of prostate cancer recurrence after radical prostatectomy  , external beam radiation therapy and brachytherapy . MATERIAL S AND METHODS This study was done in 1,153 men treated with radical prostatectomy , external beam radiation therapy and brachytherapy who had clinical stage T1-T2c prostate adenocarcinoma and participated in the CaPSURE Diet and Lifestyle sub study by completing the semiquantitative Food Frequency Question naire in 2004 to 2005 .  We used Cox proportional hazards regression to analyze the association between folate intake and prostate cancer progression . RESULTS Prostate cancer progressed in 101 men ( 8.76 % ) during a mean 34-month followup . After multivariate adjustment we observed no evidence of an association of the intake of total folate , dietary folate or dietary folate equivalents with prostate cancer recurrence . On secondary analysis by treatment after radical prostatectomy patients in the lowest decile of dietary folate intake had a 2.6-fold increase in the risk of recurrence ( HR 2.56 , 95 % CI 1.23 - 5.29 , p = 0.01 ) . In patients treated with external beam radiation and brachytherapy we observed no evidence of an association between prostate cancer progression and increased folate intake . CONCLUSIONS Results suggest that the consumption of foods and multivitamins that contain folate is not associated with prostate cancer progression after definitive treatment Background : Protective effects have been suggested for digoxin against prostate cancer risk . However , few studies have evaluated the possible effects on prostate cancer-specific survival . We studied the association between use of digoxin or beta-blocker sotalol and prostate cancer-specific survival as compared with users of other antiarrhythmic drugs in a retrospective cohort study . Methods : Our study population consisted of 6537 prostate cancer cases from the Finnish R and omized Study of Screening for Prostate Cancer diagnosed during 1996–2009 ( 485 digoxin users ) . The median exposure for digoxin was 480 DDDs ( interquartile range 100–1400 DDDs ) . During a median follow-up of 7.5 years after diagnosis , 617 men ( 48 digoxin users ) died of prostate cancer . We collected information on antiarrhythmic drug purchases from the national prescription data base . Both prediagnostic and postdiagnostic drug usages were analysed using the Cox regression method . Results : No association was found for prostate cancer death with digoxin usage before ( HR 1.00 , 95 % CI 0.56–1.80 ) or after ( HR 0.81 , 95 % CI 0.43–1.51 ) prostate cancer diagnosis . The results were also comparable for  sotalol and antiarrhythmic drugs  in general . Among men not receiving hormonal therapy , prediagnostic digoxin usage was associated with prolonged prostate cancer survival ( HR 0.20 , 95 % CI 0.05–0.86 ) . Conclusions : No general protective effects against prostate cancer were observed for digoxin or sotalol usage High-temperature cooked meat contains heterocyclic amines , including 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine ( PhIP ) , and polycyclic aromatic hydrocarbons , such as benzo(a)pyrene ( BaP ) . In rodents , a high intake of PhIP induces prostate tumors . We prospect ively investigated the association between meat and meat mutagens , specifically PhIP , and prostate cancer risk in the Prostate , Lung , Colorectal , and Ovarian Cancer Screening Trial . Diet was assessed using a 137-item food frequency question naire and a detailed meat-cooking question naire linked to a data base for BaP and the heterocyclic amines 2-amino-3,8-dimethylimidazo[4,5-b]quinoxaline ( MeIQx ) , 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline ( DiMeIQx ) , and PhIP . During follow-up , we ascertained a total of 1,338 prostate cancer cases among 29,361 men ; of these , 868 were incident cases ( diagnosed after the first year of follow-up ) and 520 were advanced cases ( stage III or IV or a Gleason score of > or = 7 ) . Total , red , or white 
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For some risk factors , evidence was insufficient to assess potential effects , while for others there was no evidence of an effect .
For selected risk factors , namely metformin , aspirin and statin use , diabetes , obesity , and specific dietary intakes , there was low- quality evidence of modest effects on PCa risk .
We found that for some factors data are currently insufficient to make definitive conclusions , while for others available studies seem to indicate an effect on the risk of prostate cancer