Kinetics of the incorporation of dietary fatty acids into serum cholesteryl esters, erythrocyte membranes, and adipose tissue: an 18-month controlled study. A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Issues related to the conduct of systematic reviews: a focus on the nutrition field. Dietary fat intake and risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. Incorporation of eicosapentaenoic and docosahexaenoic acids into lipid pools when given as supplements providing doses equivalent to typical intakes of oily fish1234 Serum phospholipid fatty acids, genetic variation in myeloperoxidase, and prostate cancer risk in heavy smokers: a gene-nutrient interaction in the carotene and retinol efficacy trial. The role of prostate-specific antigen (PSA) testing patterns in the recent prostate cancer incidence declinein the United States Determinants of Erythrocyte Omega‐3 Fatty Acid Content in Response to Fish Oil Supplementation: A Dose–Response Randomized Controlled Trial Plasma phospholipid fatty acids, dietary fatty acids and prostate cancer risk A Prospective Study of Dietary Alpha-linolenic Acid and the Risk of Prostate Cancer (United States) A prospective study of dietary fat and risk of prostate cancer. n-3 fatty acids and cardiovascular events after myocardial infarction.
Tissue levels of n-3 fatty acids reflect dietary intake , but quantitative data about rate of incorporation and levels as a function of intake are scarce . We fed 58 men 0 , 3 , 6 , or 9 g/d of fish oil for 12 months and monitored fatty acids in serum cholesteryl esters , erythrocytes , and subcutaneous fat during and after supplementation .  Eicosapentaenoic acid ( EPA ) in cholesteryl esters plateaued after 4 - 8 weeks ; the incorporation half-life was 4.8 days . Steady-state levels increased by 3.9 + /- 0.3 mass % points ( + /- SE ) for each extra gram of EPA eaten per day . Incorporation of docosahexaenoic acid ( DHA ) was erratic ; plateau values were 1.1 + /- 0.1 mass % higher for every g/d ingested . Incorporation of EPA into erythrocyte membranes showed a half-life of 28 days ; a steady state was reached after 180 days . Each g/d increased levels by 2.1 + /- 0.1 mass % . C22:5n-3 levels increased markedly . Changes in DHA were erratic and smaller . EPA levels in adipose tissue rose also ; the change after 6 months was 67 % of that after 12 months in gluteal and 75 % in abdominal fat . After 12 months each gram per day caused an 0.11 + /- 0.01 mass % rise in gluteal fat for EPA , 0.53 + /- 0.07 for C22:5n-3 , and 0.14 + /- 0.03 for DHA . Thus , different ( n-3 ) fatty acids were incorporated with different efficiencies , possibly because of interconversions or different affinities of the enzymatic pathways involved . EPA levels in cholesteryl esters reflect intake over the past week or two , erythrocytes over the past month or two , and adipose tissue over a period of years . These findings may help in assessing the intake of ( n-3 ) fatty acids in epidemiological studies 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 Systematic review s ( SRs ) are an increasingly popular evidence -based tool and are often used to answer complex research questions across many different research domains . Early SR methodology was advanced by social scientists , and the term meta- analysis was coined by a social scientist who also conducted research in psychology . SRs have recently become popular in healthcare and are likely to be beneficial in any field . The aim of this report is to highlight issues in SR conduct with a focus on the field of nutrition and to make recommendations on improving SR conduct in this area . Development of the research question is probably the most important step in conducting an SR . The 4 main components of an answerable question are 1 ) the patient , population , or problem ; 2 ) the intervention , independent variable , or exposure ; 3 ) the comparators ; and 4 ) the dependent variables or outcomes of interest . The question will be used to determine the optimal methods for conducting the SR . SRs often include study design s beyond r and omized trials and do not always include a meta- analysis of the results . Other topics explored include underst and ing and interpreting discordant review s and the importance of reporting tools [ eg , QUality Of Reporting Of Meta-analyses ( QUOROM Statement ) or CONsoli date d St and ards Of Reporting of Trials ( CONSORT Statement ) ] . Recommendations are then provided , such as developing a capacity-building program , search ing the primary literature for research gaps , and extending reporting tools such as the QUOROM Statement to the field of nutrition BACKGROUND Findings from early observational studies have suggested that the intake of dietary fat might be a contributing factor in the etiology of prostate cancer . However , the results from more recent prospect i ve studies do not support this hypothesis , and the possible association between different food sources of fat and prostate cancer risk also remains unclear . OBJECTIVE The objectives were to assess whether intakes of dietary fat , subtypes of fat , and fat from animal products were associated with prostate cancer risk . DESIGN This was a multicenter prospect i ve study of 142,520 men in the European Prospect i ve Investigation into Cancer and Nutrition ( EPIC ) . Dietary fat intake was estimated with the use of country-specific vali date d food question naires . The association between dietary fat and risk of prostate cancer was assessed by using Cox regression , stratified by recruitment center and adjusted for height , weight , smoking , education , marital status , and energy intake . RESULTS After a median follow-up time of 8.7 y , prostate cancer was diagnosed in 2727 men . There was no significant association between dietary fat ( total , saturated , monounsaturated , and polyunsaturated fat and the ratio of polyunsaturated to saturated fat ) and risk of prostate cancer . The hazard ratio for prostate cancer for the highest versus the lowest quintile of total fat intake was 0.96 ( 95 % CI : 0.84 , 1.09 ; P for trend = 0.155 ) . There were no significant associations between prostate cancer risk and fat from red meat , dairy products , and fish . CONCLUSION The results from this large multicenter study suggest that there is no association between dietary fat and prostate cancer risk 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 Background : Estimation of the intake of oily fish at a population level is difficult . The measurement of eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) in biological sample s may provide a useful biomarker of intake . Objective : We identified the most appropriate biomarkers for the assessment of habitual oily fish intake and changes in intake by elucidating the dose- and time-dependent response of EPA and DHA incorporation into various biological sample s that represent roles in fatty acid transport , function , and storage . Design : This was a double-blind , r and omized , controlled intervention trial in 204 men and women that lasted 12 mo .  EPA and DHA capsules were provided in a manner to reflect sporadic consumption of oily fish ( ie , 1 , 2 , or 4 times/wk ) .  EPA and DHA  were assessed at 9 time points over 12 mo in 9 sample types ( red blood cells , mononuclear cells , platelets , buccal cells , adipose tissue , plasma phosphatidylcholine , triglycerides , cholesteryl esters , and nonesterified fatty acids ) . Results : A dose response ( P < 0.05 ) was observed for EPA and DHA in all pools except for red blood cell EPA ( P = 0.057 ) . EPA and DHA measures in plasma phosphatidylcholine and platelets were best for the discrimination between different intakes ( P < 0.0001 ) . The rate of incorporation varied between sample types , with the time to maximal incorporation ranging from days ( plasma phosphatidylcholine ) to months ( mononuclear cells ) to > 12 mo ( adipose tissue ) . Conclusions : Plasma phosphatidylcholine EPA plus DHA was identified as the most suitable biomarker of acute changes in  EPA and DHA intake , and platelet and mononuclear cell EPA plus DHA were the most suitable biomarkers of habitual intake . This trial was registered at Current Controlled Trials ( www.controlled-trials.com ) as IS RCT N48398526 The authors investigated associations of serum phospholipid n-3 and n-6 polyunsaturated fatty acids ( PUFAs ) and trans-fatty acids with prostate cancer risk , and whether myeloperoxidase G-463A ( rs2333227 ) modified the associations in the Carotene and Retinol Efficacy Trial ( CARET ) ( Seattle , Washington ; Irvine , California ; New Haven , Connecticut ; San Francisco , California ; Baltimore , Maryl and ; and Portl and , Oregon , 1985 - 2003 ) . Prer and omization sera were assayed for  fatty acids  among 641 men with incident prostate cancer ( 368 nonaggressive and 273 aggressive ( stage III/IV or Gleason score ≥7 ) ) and 1,398 controls . Overall , dihomo-γ-linolenic ( quartiles 4 vs. 1 : odds ratio ( OR ) = 0.66 , 95 % confidence interval ( CI ) : 0.49 , 0.95 ; P(trend ) = 0.024 ) and docosatetraenoic ( OR = 0.69 , 95 % CI : 0.46 , 1.02 ; P(trend ) = 0.011 ) acids were inversely associated with nonaggressive and aggressive prostate cancer risks , respectively . Among men with MPO GG , the genotype upregulating oxidative stress , quartiles 4 versus 1 eicosapentaenoic plus docosahexaenoic acids were suggestively associated with an increased risk of aggressive prostate cancer ( OR = 1.66 , 95 % CI : 0.95 , 2.92 ; P(trend ) = 0.07 ) . However , the association was the inverse among men with MPO GA/AA genotypes ( P(interaction ) = 0.011 ) . Interactions were also observed for docosapentaenoic acid , total n-3 PUFAs , and arachidonic acid . MPO GA/AA vs. GG was associated with a 2-fold increase in aggressive prostate cancer risk among men with low ( quartile 1 ) n-3 PUFAs . This study adds important evidence linking oxidative stress with prostate carcinogenesis Objectives : Trends in first-time and later PSA procedure rates are ascertained using longitudinal data from a population -based cohort . These trends are compared to trends in prostate cancer incidence to determine the role of PSA in the recent decline in prostate cancer incidence . Methods : Medicare data were linked with tumor registry data from the National Cancer Institute 's Surveillance , Epidemiology , and End Results ( SEER ) Program . A 5 percent r and om sample ( n=39985 ) of Medicare beneficiaries from the SEER areas without a previous diagnosis of prostate cancer as of January 1 , 1988 was followed through 1994 . Trends in first-time PSA use were distinguished from those of second or later for men without diagnosed prostate cancer . Results : Trends in the rate of first-time PSA procedures track closely with trends in prostate cancer incidence rates , increasing until 1992 and decreasing thereafter . Similar patterns were observed by race and age group . Geographic variability in the dissemination of PSA screening was observed , yet the association between testing and incidence remained . Men in the cohort had a 4.7 percent chance of being diagnosed within three months of an initial PSA test , with the percentage falling for subsequent tests . Conclusions : It is informative to distinguish first from later tests when assessing the effect of the diffusion of a test in a population . Taking this approach was useful in illuminating the role of PSA testing in a reversal of a long-term increase in prostate cancer incidence rates Background The erythrocyte membrane content of eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) , which constitutes the omega‐3 index ( O3I ) , predicts cardiovascular disease mortality . The amount of EPA+DHA needed to achieve a target O3I is poorly defined , as are the determinants of the O3I response to a change in EPA+DHA intake . The objective of this study was to develop a predictive model of the O3I response to EPA+DHA supplementation in healthy adults , specifically identifying factors that determine the response . Methods and Results A r and omized , placebo‐controlled , double‐blind , parallel‐group study was conducted in 115 healthy men and women . One of 5 doses ( 0 , 300 , 600 , 900 , 1800 mg ) of EPA+DHA was given daily as placebo or fish oil supplements for ≈5 months . The O3I was measured at baseline and at the end of the study . There were no significant differences in the clinical characteristics between the groups at baseline . The O3I increased in a dose‐dependent manner ( P<0.0001 ) , with the dose of EPA+DHA alone accounting for 68 % ( quadratic , P<0.0001 ) of the variability in the O3I response . Dose adjusted per unit body weight ( g/kg ) accounted for 70 % ( linear , P<0.0001 ) . Additional factors that improved prediction of treatment response were baseline O3I , age , sex , and physical activity . Collectively , these explained 78 % of the response variability ( P<0.0001 ) . Conclusions Our findings vali date the O3I as a biomarker of EPA+DHA consumption and identify additional factors , particularly body weight , that can be used to tailor EPA+DHA recommendations to achieve a target O3I Animal and experimental studies have demonstrated that long‐chain n‐3 fatty acids inhibit the development of prostate cancer , whereas n‐6 fatty acids might promote it . We performed a case – cohort analysis within the Melbourne Collaborative Cohort Study using a r and om sample of 1,717 men and 464 prostate cancer cases to investigate associations between fatty acids assessed in plasma phospholipids ( PPLs ) or diet ( estimated using a 121‐item food frequency question naire ) and prostate cancer risk . Hazard ratios ( HRs ) and 95 % confidence intervals ( CIs ) were estimated using Cox regression . Prostate cancer risk was positively associated with % PPL saturated fatty acids ( SFAs ) ; HR [ 95 % CI ] = 1.51 [ 1.06 , 2.16 ] ( Q5 vs. Q1 , fifth vs. first quintile ) ; p‐trend = 0.003 . HRs ( Q5 to Q2 vs. Q1 ) were significantly elevated for % PPL palmitic acid . % PPL oleic acid was inversely associated with risk , HR = 0.62 [ 0.43 , 0.91 ] ( Q5 vs. Q1 ) ; p‐trend = 0.04 . No statistically significant linear trends were observed for dietary intakes . The HRs were elevated for moderate intakes of linoleic acid ( Q2 and Q3 vs. Q1 , 1.58 [ 1.10 , 2.28 ] and 1.70 [ 1.18 , 2.46 ] , respectively ) , but the increase was not significant for higher intakes ( Q4 and Q5 ) . No association varied significantly by tumour aggressiveness ( all p‐homogeneity > 0.1 ) . Prostate cancer risk was positively associated with % PPL SFA , largely attributable to palmitic acid and inversely associated with % PPL monounsaturated fatty acids , largely attributable to oleic acid . Higher risks were also observed for dietary n‐6 polyunsaturated fats , primarily linoleic acid Background Alpha-linolenic acid ( ALA ) is the most common omega-3 fatty acid in the Western diet . The relation of dietary intake of ALA to prostate cancer risk remains unresolved . Objective We prospect ively evaluated total ALA and ALA from specific food sources including animal , fish , and plant sources in relation to prostate cancer risk . Design A cohort of 29,592 male participants ( age 55–74 years ) in the screening arm of the Prostate , Lung , Colorectal , and Ovarian ( PLCO ) Cancer Screening Trial was followed for an average of 5.1 years . Results We ascertained 1,898 cases of total prostate cancer , of which 1,631 were organ-confined cases ( stage T1b to T3a and N0M0 ) and 285 were advanced stage cases ( stage≥T3b , N1 , or M1 ) . We found no association between total ALA intake and overall prostate cancer ( multivariate RR comparing extreme quintiles=0.94 ; 95 % CI=0.81–1.09 ; P for trend=0.76 ) . The corresponding RRs for organ-confined and advanced prostate cancer were 0.94 ( 95 % CI=0.80–1.10 ; P for trend=0.80 ) and 0.83 ( 95 % CI=0.58–1.19 ; P for trend=0.34 ) , respectively . In addition , no relations were observed between ALA intake from any specific food source and the risks of total , organ-confined , or advanced prostate cancer . ALA intake also showed no association with low grade ( Gleason sum<7 ; 1,221 cases ) tumors ( P for trend=0.23 ) or high grade ( Gleason sum≥7 ; n=677 cases ) tumors ( P for trend=0.26 ) . Conclusions In this prospect i ve study of predominantly Caucasian men who were screened annually for newly incident prostate cancer , dietary intake of total ALA and ALA from specific food sources was not associated with risk of total prostate cancer or prostate tumors that were defined by stage and grade BACKGROUND The strong correlation between national consumption of fat and national rate of mortality from prostate cancer has raised the hypothesis that dietary fat increases the risk of this malignancy . Case-control and cohort studies have not consistently supported this hypothesis . PURPOSE We examined prospect ively the relationship between prostate cancer and dietary fat , including specific fatty acids and dietary sources of fat . We examined the relationship of fat consumption to the incidence of  advanced prostate cancer ( stages C , D , or fatal cases ) and to the total incidence of prostate cancer . METHODS We used data from the Health Professionals Follow-up Study , which is a prospect i ve cohort of 51529 U.S. men , aged 40 through 75 , who completed a vali date d food-frequency question naire in 1986 . We sent follow-up question naires to the entire cohort in 1988 and 1990 to document new cases of a variety of diseases and to up date exposure information . As of January 31 , 1990 , 300 new cases of prostate cancer , including 126 advanced cases , were documented in 47855 participants initially free of diagnosed cancer . The Mantel-Haenszel summary estimator was used to adjust for age and other potentially confounding variables . Multiple logistic regression was used to estimate relative risks ( RRs ) when controlling simultaneously for more than two covariates . RESULTS Total fat consumption was directly related to risk of advanced prostate cancer ( age- and energy-adjusted RR = 1.79 , with 95 % confidence interval [ CI ] = 1.04 - 3.07 , for high versus low quintile of intake ; P [ trend ] = .06 ) . This association was due primarily to animal fat ( RR = 1.63 ; 95 % CI = 0.95 - 2.78 ; P [ trend ] = .08 ) , but not vegetable fat . Red meat represented the food group with the strongest positive association with advanced cancer ( RR = 2.64 ; 95 % CI = 1.21 - 5.77 ; P = .02 ) . Fat from dairy products ( with the exception of butter ) or fish was unrelated to risk . Saturated fat , monounsaturated fat , and alpha-linolenic acid , but not linoleic acid , were associated with advanced prostate cancer risk ; only the association with alpha-linolenic acid persisted when saturated fat , monounsaturated fat , linoleic acid , and alpha-linolenic acid were modeled simultaneously ( multivariate RR = 3.43 ; 95 % CI = 1.67 - 7.04 ; P [ trend ] = .002 ) . CONCLUSION The results support the hypothesis that animal fat , especially fat from red meat , is associated with an elevated risk of advanced prostate cancer . IMPLICATION S These findings support recommendations to lower intake of meat to reduce the risk of prostate cancer . The potential roles of carcinogens formed in cooking animal fat and of alpha-linolenic acid in the progression of prostate cancer need to be explored BACKGROUND Results from prospect i ve cohort studies and r and omized , controlled trials have provided evidence of a protective effect of n-3 fatty acids against cardiovascular diseases . We examined the effect of the marine n-3 fatty acids eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) and of the plant-derived alpha-linolenic acid ( ALA ) on the rate of cardiovascular events among patients who have had a myocardial infa rct ion . METHODS In a multicenter , double-blind , placebo-controlled trial , we r and omly assigned 4837 patients , 60 through 80 years of age ( 78 % men ) , who had had a myocardial infa rct ion and were receiving state-of-the-art antihypertensive , antithrombotic , and lipid-modifying therapy to receive for 40 months one of four trial margarines : a margarine supplemented with a combination of EPA and DHA ( with a targeted additional daily intake of 400 mg of EPA-DHA ) , a margarine supplemented with ALA ( with a targeted additional daily intake of 2 g of ALA ) , a margarine supplemented with EPA-DHA and ALA , or a placebo margarine . The primary end point was the rate of major cardiovascular events , which comprised fatal and nonfatal cardiovascular events and cardiac interventions . Data were analyzed according to the intention-to-treat principle , with the use of Cox proportional-hazards models . RESULTS The patients consumed , on average , 18.8 g of margarine per day , which result ed in additional intakes of 226 mg of EPA combined with 150 mg of DHA , 1.9 g of ALA , or both , in the active-treatment groups . During the follow-up period , a major cardiovascular event occurred in 671 patients ( 13.9 % ) . Neither EPA-DHA nor ALA reduced this primary end point ( hazard ratio with EPA-DHA , 1.01 ; 95 % confidence interval [ CI ] , 0.87 to 1.17 ; P=0.93 ; hazard ratio with ALA , 0.91 ; 95 % CI , 0.78 to 1.05 ; P=0.20 ) . In the prespecified subgroup of women , ALA , as compared with placebo and EPA-DHA alone , was associated with a reduction in the rate of major cardiovascular events that approached significance ( hazard ratio , 0.73 ; 95 % CI , 0.51 to 1.03 ; P=0.07 ) . The rate of adverse events did not differ significantly among the study groups . CONCLUSIONS Low-dose supplementation with EPA-DHA or ALA did not significantly reduce the rate of major cardiovascular events among patients who had had a myocardial infa rct ion and who were receiving state-of-the-art antihypertensive , antithrombotic , and lipid-modifying therapy . ( Funded by the Netherl and s Heart Foundation and others ; Clinical Trials.gov number , NCT00127452 . )
We conducted a systematic review and meta- analysis to estimate the potential association between LCω-3PUFAs and  prostate cancer ( PC ) .