Psa Just Eat Meat, That's All You Have to Eat, Have Some Beef or Fish or Eggs
Am J Clin Nutr. 2010 Mar; 91(iii): 712–721.
Intakes of meat, fish, poultry, and eggs and take a chance of prostate cancer progressionone, two, three, iv
Received 2009 Jul 7; Accepted 2009 December 11.
Abstract
Groundwork: Processed meat and fish have been shown to be associated with the chance of advanced prostate cancer, but few studies take examined diet after prostate cancer diagnosis and take a chance of its progression.
Objective: We examined the association betwixt postdiagnostic consumption of candy and unprocessed red meat, fish, poultry, and eggs and the risk of prostate cancer recurrence or progression.
Design: We conducted a prospective study in 1294 men with prostate cancer, without recurrence or progression as of 2004–2005, who were participating in the Cancer of the Prostate Strategic Urologic Enquiry Endeavor and who were followed for an boilerplate of ii y.
Results: We observed 127 events (prostate cancer decease or metastases, elevated prostate-specific antigen concentration, or secondary handling) during 2610 person-years. Intakes of candy and unprocessed red meat, fish, total poultry, and skinless poultry were not associated with prostate cancer recurrence or progression. Greater consumption of eggs and poultry with skin was associated with 2-fold increases in chance in a comparison of extreme quantiles: eggs [hazard ratio (Hour): ii.02; 95% CI: 1.x, 3.72; P for trend = 0.05] and poultry with skin (Hour: 2.26; 95% CI: 1.36, 3.76; P for trend = 0.003). An interaction was observed between prognostic take chances at diagnosis and poultry. Men with high prognostic adventure and a loftier poultry intake had a 4-fold increased risk of recurrence or progression compared with men with depression/intermediate prognostic hazard and a depression poultry intake (P for interaction = 0.003).
Conclusions: Our results suggest that the postdiagnostic consumption of processed or unprocessed red meat, fish, or skinless poultry is not associated with prostate cancer recurrence or progression, whereas consumption of eggs and poultry with pare may increase the risk.
INTRODUCTION
Approximately 2.1 meg men currently alive with prostate cancer in the U.s., and an estimated 186,000 new cases were diagnosed in 2008. Over xc% of new cases are diagnosed in the localized or regional stages and have a 5-y survival approaching 100%. In contrast, the 5-y survival of prostate cancer patients with afar metastases is only 32% (i). Thus, identification of modifiable factors that bear upon the progression of prostate cancer is important for prostate cancer patients and public wellness.
Prostate cancer is a heterogeneous disease, and factors that touch on its occurrence may differ from factors that affect its progression. For example, processed or cured meats are more strongly associated with increased run a risk of avant-garde or metastatic prostate cancer than of total prostate cancer (2–8). Similarly, fish intake may not be associated with risk of total prostate cancer, but is inversely associated with risk of metastatic prostate cancer and prostate cancer mortality (ix, 10). Fewer prospective studies have assessed poultry or egg consumption and prostate cancer take chances, and the results accept been largely inconclusive, and no studies have examined postdiagnostic intake of these items in relation to prostate cancer progression (11–13).
In addition, saturated fat intake may be positively associated with prostate cancer mortality or biochemical recurrence after radical prostatectomy, and we previously reported a decreased run a risk of prostate cancer progression associated with high postdiagnostic fish and lycopersicon esculentum sauce intake in the Health Professionals Follow-Up Written report (14–17). These findings support the hypothesis that dietary factors may touch on the progression of prostate cancer.
The aim of this written report was to prospectively analyze the associations between postdiagnostic processed and unprocessed red meat, fish, poultry, and egg consumption and the gamble of prostate cancer recurrence or progression in the Diet and Lifestyle substudy of the Cancer of the Prostate Strategic Urologic Research Endeavor [CapSURE (CapSURE is a trademarked proper noun)]. We hypothesized that consumption of unprocessed and processed red meat may increase the risk of prostate cancer recurrence or progression because of the loftier saturated fat content of such meats (18) and that consumption of fish may decrease the risk of recurrence or progression through benign furnishings on inflammatory pathways (19). For comparing, we examined poultry and eggs—animal products with lower levels of saturated fat and long chain due north−3 fatty acids—and hypothesized that consumption of these foods would not exist associated with prostate cancer recurrence or progression.
SUBJECTS AND METHODS
Study population
Men in this written report were participants in the Diet and Lifestyle substudy of CaPSURE. Details of CaPSURE were published previously (20, 21). Starting in 1995, men with biopsy-proven prostate cancer were invited to participate at 31 sites throughout the U.s.a. and asked to complete a questionnaire on sociodemographic characteristics, comorbidities, health-related quality of life, and employ of health services. Follow-upward questionnaires were mailed every 6 mo. Clinical information were collected by a certified urologist at baseline and at each subsequent clinic visit, including history of prostate cancer diagnosis, biopsies, pathological results, and treatments. During 2004 and 2005, active members at 25 CaPSURE sites were invited to participate in the Diet and Lifestyle substudy. Invitations were mailed to 5570 participants, and 2467 participants accepted. The baseline survey included questions on sociodemographic factors, medical history, physical activeness, and a semiquantitative food-frequency questionnaire (FFQ). The distribution of sociodemographic and prognostic factors did non differ across the 25 CaPSURE sites. Completed surveys were received from 87% of the men who accustomed the invitation. This report was approved past the Committee on Human Research, the Institutional Review Lath of the University of California, San Francisco.
Dietary cess
The FFQ included 127 food and drink items plus supplements. A portion size was specified for each item, and participants were asked how ofttimes they had consumed that amount of the item on average over the past twelvemonth (<1 time/mo, i–three times/mo, 1 time/wk, 2–four times/wk, five–half dozen times/wk, 1 time/d, 2–3 times/d, four–five times/d, or ≥6 times/d). Intake of each food item was calculated by multiplying the frequency of consumption by the portion size specified. Participants were asked whether they consumed less, the aforementioned amount, or more of each food detail relative to before their diagnosis of prostate cancer. Additional questions addressed the type of fatty used when cooking, the frequency of fried food consumption, and an open-ended section for any foods eaten frequently that were not included in the multiple-choice section.
We divers 5 food groups for this assay: candy ruddy meat, unprocessed red meat, fish, poultry, and eggs. Candy red meat included hot dogs, salary, and processed meats (bologna, salami, sausage, etc). Unprocessed blood-red meat included hamburgers, liver, beef, pork, or lamb every bit a sandwich or mixed dish (stew, goulash, lasagna, etc), and beef, pork, or lamb as a main dish (steak, roast, ham, etc). Fish included canned tuna fish, dark-meat fish (salmon, mackerel, bluefish, swordfish, sardines, etc), other fish, and shrimp, lobster, or scallops equally a main dish. Poultry included skinless chicken or turkey and chicken or turkey with peel. We included eggs as a separate category because their nutrient composition differs from that of other poultry products.
Result assessment and follow-up
Data on prostate cancer progression were collected from medical records by report investigators and included pathologic results, staging, and master and subsequent treatments. After receiving the participants' permission, self-reported hospitalizations were verified through hospital records. Procedures performed, length of stay, discharge diagnosis, and discharge condition were recorded. The National Expiry Index and Bureau of Vital Statistics were checked through x July 2008 for bloodshed data, and records were reviewed by a report doc to verify the date, main cause, and location of expiry.
We used the post-obit clinical variables from physicians' reports: diagnostic biopsy Gleason sum (2–ten), prostate-specific antigen (PSA) at diagnosis (0-ten.0, x.i–twenty.0, or > xx.0 ng/mL), clinical T stage at diagnosis (T1, T1a-c; T2, T2a-c; T3, T3a-c, T4, T4a-b), and primary and subsequent treatments. Treatments were categorized as follows: radical prostatectomy (RP), radiation therapy (RT), hormone therapy (ADT), and other. Other treatments included cryosurgery, trans-urethral microwave thermotherapy, second line medications, and watchful waiting. Watchful waiting was included in "other treatment" because information technology was uncommon in this study population (n = 47, 3.six%). Nosotros categorized each participant by prognostic risk based on the D'Amico risk categories as follows (22): loftier (PSA > 20 ng/mL or Gleason sum = 8–10 or T stage T3a+), intermediate [PSA = x.1–20 ng/mL or Gleason sum = 7 or secondary 4–5 pattern or T stage T2b/T2c (2002) or T2b (1997)], or low (PSA ≤ 10 ng/mL and Gleason sum = 2–6 and T phase = T1/T2a).
We defined an upshot of prostate cancer recurrence or progression (hereafter referred to as "progression" for brevity) as the first of the following events: prostate cancer death, os metastases from prostate cancer, biochemical recurrence, or initiation of secondary treatment. An outcome of bone metastases was defined as physician study of 1) distant prostate cancer progression to os, 2) a positive os scan, 3) radiation for metastasis at a bone site, or 4) M1b stage in TNM staging. Biochemical recurrence was divers as 2 consecutive PSA concentrations ≥0.2 ng/mL ≥8 wk after radical prostatectomy or 3 consecutive increases in PSA above the postradiation nadir afterward radiations therapy. Secondary treatment was defined as treatment initiated ≥6 mo later on primary treatment ended. Secondary treatment was included in our outcome definition because, among men who have undergone main handling, initiation of secondary treatment is indicative of biochemical or clinical evidence of affliction recurrence (23, 24). The date of prostate cancer progression was assigned as the first of the post-obit: prostate cancer death, diagnosis of bone metastases from prostate cancer, date of second PSA increase for radical prostatectomy patients, midpoint betwixt date of postradiation nadir and first PSA increase for radiation patients, or date of initiation of secondary handling.
Analysis population and exclusion criteria
To be included in this analysis, men had to have completed the baseline Nutrition and Lifestyle CaPSURE survey between April 2004 and November 2005 (due north = 2134). We excluded men with avant-garde or metastatic disease at diagnosis (northward = 139) and men with no treatment information (n = 36). We also excluded men with no follow-upward beyond their Diet and Lifestyle survey (n = 251) and men whose prostate cancer progressed before they completed the survey (north = 365). Last, we excluded men who reported an unreasonable free energy intake (<800 or >4200 kcal/d) (n = 49), which resulted in 1294 men for analysis.
Statistical methods
We analyzed the associations between the four meat groups and eggs and time to prostate cancer progression using Cox proportional gamble regression models. We used hazards ratios (HRs) and 95% CIs to estimate the relative risk of progression. Person-time was calculated for each participant from the date they completed the Diet and Lifestyle questionnaire until the date of illness progression, nonprostate cancer decease, last contact, or cease of follow-upward (10 July 2008), whichever occurred first. Dietary intakes were divided into quantiles based on the distribution of intakes in the study population. Relative risks were calculated by comparison the risk of progression for men in the upper quantiles relative to men in the lowest quantile.
Our bones model included indicator variables for the quartiles of the food grouping or item of interest, age at diagnosis (<threescore, 60–69.ix, seventy–79.nine, or ≥fourscore y), energy intake (kcal/d), and fourth dimension from diagnosis to questionnaire. Our second model additionally adjusted for predictors of progression in this report population, including primary treatment (RP, RT, ADT, or other), body mass index (BMI; in kg/ktwo; <eighteen.five, 18.5–24.9, 25–29.9, or ≥30), nonvigorous activity (metabolic equivalent hours/wk), Gleason sum at diagnosis (2–x), and PSA at diagnosis (0–10.0, 10.1–20.0, or >twenty.0 ng/mL). We examined models adjusting for other nutrient groups (meats other than the main exposure, fruit, grains, sweets, vegetables, and dairy products), clinical T stage at diagnosis, smoking, race, pedagogy, income, marital status, vigorous action, and frequency of fried food intake in addition to the abovementioned variables, and our results did not change materially. In addition, we considered confounding by love apple products and cruciferous vegetables, because these items have been shown to exist inversely associated with prostate cancer incidence or progression in prior studies; however, the results were unaffected (14, xv, 17, 25, 26). Nosotros added energy-adapted saturated fatty to our final models using the nutrient residual method to examine whether saturated fat from the nutrient grouping of involvement explained any of the association between the nutrient group and prostate cancer progression (27). Concluding, nosotros used the median value of each quantile as an ordinal score variable to test for evidence of linear trends in our final models (28).
Nosotros examined whether the associations for whatever meat group or eggs and risk of progression were modified by BMI, prognostic risk at diagnosis, or time from diagnosis to questionnaire. BMI was considered as a potential effect modifier based on Strom et al (fifteen), who observed shorter progression-free survival after prostatectomy among obese men who consumed a high-saturated-fat nutrition earlier diagnosis compared with lean men who consumed a loftier-saturated-fat diet earlier diagnosis. Nosotros considered effect modification past prognostic risk because prostate cancer has a heterogeneous natural history, and we hypothesized that dietary factors may accept a dissimilar clan with progression of ambitious compared with nonaggressive prostate cancer. We generated cross-production terms between each detail and potential effect modifier, entered the cross-product terms in our multivariate models, and tested the significance of the cross-product terms' regression coefficients using Wald tests (29). If there was evidence of a pregnant interaction, we created indicator variables for each unique combination of issue modifier and quartile of meat or egg intake and included them in a multivariate model to compare the risk of progression in each group with a common reference.
To assess whether our results were affected past reverse causation (ie, higher-risk patients ate more or less of a nutrient detail after their diagnosis than did lower-risk patients out of business organisation for their affliction prognosis), we compared self-reported alter in consumption of private meat and egg items after prostate cancer diagnosis across prognostic risk categories using Pearson chi-foursquare and Fisher's verbal tests.
We were concerned that health-conscious men would choose healthier diets and would also be more likely to have routine PSA monitoring and/or seek secondary treatment. Information technology was possible that the inclusion of biochemical recurrence and second treatment in our outcome definition would introduce positive misreckoning between healthy dietary factors and chance of progression and negative misreckoning between unhealthy dietary factors and risk of progression. To address this possibility, we performed secondary analyses excluding events defined by initiation of secondary handling, of which nosotros had no biological show of recurrence preceding the secondary treatment (n = 38); our results did not modify materially. We divers biological evidence of recurrence as any PSA concentration ≥0.2 ng/mL subsequently radical prostatectomy or whatsoever PSA concentration ≥0.iii ng/mL in a higher place the posttreatment nadir later on radiation or other forms of treatment.
Nosotros were also concerned that watchful waiters could be misclassified as events of progression if they initiated treatment during follow-upward because of anxiety rather than because of an objective modify in their disease country. Withal, our effect estimates were materially unchanged later excluding watchful waiters (northward = 47). Therefore, the results reported include all 127 events for the 1294 men. Statistical tests were ii-sided and were performed at the 0.05 level of significance. We used SAS (version 9.i; SAS Institute, Cary, NC) for all analyses.
RESULTS
We identified 127 events of prostate cancer progression amid 1294 men with a diagnosis of localized or regional prostate cancer during 2610 person-years of follow-upward. Comparing of the men included in our analysis (n = 1294) with the men who were initially invited (northward = 5570) showed that the participants were more likely to be white (95.6% compared with ninety.half dozen%), more probable to take a better prognosis (Gleason sum 2–half dozen: 68.9% compared with 63.5%; PSA 0–10 ng/mL: 83.2% compared with 74.four%), and more likely to have a radical prostatectomy as their primary treatment (63% compared with 53%). The median twelvemonth of diagnosis was 2002, and half of the participants were diagnosed between 2000 and 2003. Initiation of secondary treatment deemed for 57% (n = 72) of events, biochemical recurrence deemed for 39% (due north = 49) of events, and metastases to bone and death from prostate cancer each accounted for 2% (n = 3) of events.
A comparison of the participants' characteristics, by the highest to the lowest quartiles of the meat groups and eggs, are presented in Table 1 . Processed cherry meat and egg consumption were positively associated with less healthy lifestyle behaviors and worse clinical characteristics, including higher mean BMI, smoking, and Gleason sum 8–10 at diagnosis. Men in the highest quartile of unprocessed scarlet meat also had a higher mean BMI than did men in the lowest quartile of unprocessed red meat. Men in the highest quartiles of fish and poultry were younger at diagnosis than were men in the lowest quartiles of those items. In addition, men in the highest quartile of poultry were more likely to accept radical prostatectomy every bit their master treatment, and men in the highest quartile of fish were more likely to take other forms of handling compared with men in the lowest quartiles of those items.
Tabular array 1
Processed cerise meat | Unprocessed scarlet meat | Fish | Poultry | Eggs 2 | ||||||
Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | |
Median intake (servings/wk) three | 0 | five.0 | 0.9 | vii.0 | 0.4 | four.3 | i.0 | 5.5 | 0.iv | five.5 |
No. of participants | 310 | 337 | 324 | 303 | 348 | 347 | 380 | 346 | 319 | 176 |
Total person-years | 603 | 677 | 618 | 634 | 750 | 655 | 782 | 660 | 631 | 347 |
Age at diagnosis (y) | 65.7 ± 8.vii 4 | 65.6 ± viii.1 | 65.vii ± 7.8 | 64.6 ± eight.5 | 66.0 ± viii.2 | 64.4 ± 8.ane 5 | 67.1 ± seven.3 | 62.viii ± 8.4 v | 64.7 ± 8.0 | 64.ane ± 8.0 |
BMI (kg/m2) | 26.ii ± 3.3 | 27.ix ± 4.4 five | 26.5 ± 3.5 | 27.9 ± 4.3 5 | 27.2 ± 3.8 | 27.two ± iv.0 | 27.3 ± iii.seven | 27.eight ± 4.2 | 26.five ± three.6 | 28.3 ± 4.vii five |
Nonvigorous activity (MET-h/wk) | 11.5 ± 14.5 | 12.3 ± xv.i | eleven.v ± 13.vi | 11.7 ± 14.8 | 10.eight ± 14.5 | 12.5 ± 14.6 | 9.eight ± 13.5 | 11.9 ± 13.9 | eleven.viii ± xiv.6 | 13.0 ± 15.four |
Smoking (%) | ||||||||||
Current | 3.6 | 6.5 | 5.9 | 7.9 | 6.9 | 5.two | 6.6 | 3.eight | 6.6 | 9.7 |
By | 51.3 | 59.4 v | 52.8 | 53.5 | 49.four | 55.0 | 55.viii | 57.6 | 49.2 | 60.8 5 |
Never | 45.two | 32.i v | 41.ane | 37.three | 42.eight | 38.nine | 36.6 | 37.9 | 42.six | xxx.0 5 |
Unknown | 0.0 | 2.i 5 | 0.3 | 1.3 | 0.9 | 0.9 | one.1 | 0.9 | i.vi | 0.0 5 |
Race (%) | ||||||||||
White | 95.viii | 96.four | 93.viii | 96.0 | 97.4 | 94.0 5 | 97.1 | 94.5 | 95.3 | 96.0 |
African American | 2.3 | ii.4 | 4.6 | one.7 | 2.0 | 2.3 | one.8 | three.8 | ii.5 | 2.8 |
Other | i.nine | 1.2 | 1.5 | 2.3 | 0.6 | 3.8 5 | one.i | 1.vii | two.ii | one.1 |
Gleason sum at diagnosis (%) | ||||||||||
two–6 | 65.2 | 67.4 | 66.4 | 69.3 | 68.4 | 69.2 | 67.9 | 70.2 | 71.viii | 67.i |
7 | 28.seven | 23.four | 25.0 | 22.8 | 26.4 | 21.9 | 25.3 | 23.7 | 23.v | 21.0 |
8–ten | 4.8 | 8.0 5 | 6.8 | seven.half dozen | iv.6 | half-dozen.six | 5.5 | 4.6 | three.ane | ix.7 v |
Unknown | 1.3 | 1.two | one.nine | 0.3 | 0.six | 2.3 5 | one.three | 1.5 | 1.6 | 2.iii |
PSA at diagnosis (%) | ||||||||||
0–ten ng/mL | eighty.three | 84.nine | 81.8 | 81.9 | 84.2 | 81.8 | 82.1 | 83.2 | 84.3 | 81.3 |
ten.1–20.0 ng/mL | 12.nine | ten.one | 11.1 | 11.9 | 10.6 | 10.4 | 12.1 | eleven.0 | 10.3 | eleven.iv |
≥20 ng/mL | 3.2 | iii.ix | iv.3 | 3.iii | 2.6 | 4.three | 2.6 | three.5 | 1.ix | iii.iv |
Unknown | 3.6 | 1.2 | 2.viii | 3.0 | two.vi | 3.5 | iii.2 | two.3 | 3.five | 4.0 |
Primary treatment (%) | ||||||||||
Radical prostatectomy | 61.6 | 58.five | 61.vii | 64.0 | 60.half-dozen | 59.7 | 57.nine | 67.6 5 | 65.two | 64.8 |
Radiation therapy | 24.5 | 24.6 | 24.ane | 21.eight | 24.i | 27.4 | 25.viii | 20.two | 22.six | 22.seven |
Hormonal therapy | v.8 | vii.1 | five.6 | 5.6 | four.3 | 7.five | 7.4 | 5.viii | v.0 | vi.3 |
Other | viii.1 | 9.8 | 8.half dozen | viii.6 | 10.9 | 5.5 5 | nine.0 | six.4 | 7.two | 6.three |
A comparison of select dietary habits of the participants, past highest to lowest quartiles of the meat groups and eggs, are presented in Tabular array 2 . Afterward free energy intake was adjusted for, men in the highest quartile of processed reddish meat, unprocessed red meat, or eggs consumed more of all of these items than did men in the lowest quartiles. Men in the highest quartile of candy crimson meat also consumed more poultry and less tomato products than did men in the lowest quartile of candy cerise meat. In contrast, men in the highest quartiles of fish or poultry had healthier dietary habits, including more fish, poultry, and cruciferous vegetables, than did men in the everyman quartiles of fish or poultry. Men in the highest quartile of fish besides consumed more tomato products and less unprocessed reddish meat than did men in the lowest quartile of fish. Concluding, men in the highest quartiles of unprocessed ruddy meat, fish, or poultry consumed less dairy products than did men in the lowest quartiles of those items.
Table 2
Processed ruby meat | Unprocessed carmine meat | Fish | Poultry | Eggs 2 | ||||||
Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | Q1 | Q4 | |
No. of participants | 310 | 337 | 324 | 303 | 348 | 347 | 380 | 346 | 319 | 176 |
Full person-years | 603 | 677 | 618 | 634 | 750 | 655 | 782 | 660 | 631 | 347 |
Energy intake (kcal/d) | 1768 ± 578 3 | 2255 ± 575 4 | 1670 ± 554 | 2386 ± 598 iv | 1867 ± 641 | 2173 ± 622 4 | 1738 ± 536 | 2256 ± 632 4 | 1818 ± 615 | 2200 ± 646 4 |
Processed red meat (servings/wk) v | 0.2 ± 0.iii | 5.8 ± two.9 4 | one.vii ± 2.4 | 3.0 ± 2.7 4 | 2.v ± 2.5 | 2.half-dozen ± 2.8 | two.6 ± 2.vi | 2.half dozen ± 2.9 | 1.seven ± two.3 | iv.0 ± 3.8 four |
Unprocessed red meat (servings/wk) six | 3.0 ± 2.8 | iv.4 ± 2.iv 4 | i.ii ± 0.8 | half dozen.7 ± 2.3 4 | 4.0 ± 2.9 | three.4 ± 2.4 four | iii.7 ± 2.seven | 3.9 ± 2.5 | 3.1 ± ii.5 | 4.2 ± 2.six iv |
Fish (servings/wk) 7 | ii.4 ± 2.2 | 2.two ± one.ix | 2.five ± two.4 | 2.2 ± ii.0 | 0.6 ± 0.iv | 4.6 ± ii.1 4 | 1.7 ± i.6 | two.6 ± two.1 4 | ii.3 ± 2.iii | 2.3 ± ane.7 |
Poultry (servings/wk) 8 | iii.ii ± 2.6 | 2.5 ± 1.8 4 | 2.8 ± ii.5 | 2.8 ± two.0 | 2.3 ± 2.0 | 3.3 ± 2.three iv | 0.9 ± 0.5 | 5.0 ± ii.4 iv | two.8 ± two.iii | 3.two ± 2.6 |
Eggs (servings/wk) 9 | ii.2 ± three.4 | three.five ± 3.viii 4 | ii.4 ± 3.5 | iii.one ± 3.3 four | 2.5 ± 2.9 | 2.8 ± 3.5 | 2.iv ± two.4 | two.9 ± iii.iii | 0.3 ± 0.3 | 7.nine ± 5.three 4 |
Dairy products (servings/wk) 10 | 14.7 ± 11.3 | fourteen.iii ± eight.vii | 15.5 ± 11.ii | 12.vii ± 8.iv four | 15.seven ± eleven.3 | xiii.0 ± 8.ane 4 | 16.5 ± 11.2 | 13.one ± 8.five iv | 15.3 ± 11.iii | fourteen.9 ± eight.5 |
Love apple products (servings/wk) xi | 5.1 ± 4.1 | 4.4 ± 3.three 4 | 5.1 ± 4.3 | four.six ± 3.7 | 4.0 ± iii.3 | 5.5 ± 3.8 four | four.iii ± 3.five | 4.9 ± 3.viii | 4.7 ± 3.7 | 4.nine ± iv.ii |
Cruciferous vegetables (servings/wk) 12 | 3.2 ± 2.7 | 2.8 ± 2.viii | iii.2 ± 3.9 | iii.3 ± ii.nine | 2.2 ± 2.0 | 4.0 ± 4.0 4 | two.2 ± ii.1 | 3.6 ± 3.0 4 | 3.one ± 3.6 | 3.8 ± iii.4 |
The relative risks of prostate cancer progression by quartiles of the meat groups and eggs are presented in Tabular array iii . Nosotros observed no evidence of an clan between candy carmine meat, unprocessed red meat, or fish with prostate cancer progression. The HRs (95% CIs) for the comparing of the highest with the everyman quartiles were every bit follows: 1.30 (0.78, 2.17) for processed red meat, 0.95 (0.55, ane.66) for unprocessed red meat, and 1.13 (0.70, 1.84) for fish after adjustment for sociodemographic and clinical risk factors. We observed an increased gamble of prostate cancer progression associated with higher poultry intake that was non statistically meaning [HR for quartile 4 (Q4) compared with quartile 1 (Q1): 1.55; 95% CI: 0.91, 2.66]. In addition, we observed a significant 2-fold increased risk of prostate cancer progression among men in the highest quartile of egg intake compared with men in the lowest quartile (HR: ii.02; 95% CI: ane.x, three.72), which appeared to be limited to the highest level of intake.
Tabular array 3
Quartile of intake | |||||
1 | 2 | 3 | 4 | P for trend 2 | |
Median processed red meat intake | 0.0 | 1.0 | ii.5 | v.0 | 0.18 |
No. of events/no. of participants | 29/310 | 32/372 | 21/275 | 45/337 | |
Total person-years | 603 | 765 | 565 | 677 | |
Model 1 three | i.0 (ref) | one.01 (0.61, ane.68) 4 | 0.88 (0.50, 1.56) | 1.48 (0.91, ii.43) | |
Model 2 5 vi | one.0 (ref) | 0.91 (0.54, 1.54) | 0.89 (0.fifty, 1.61) | ane.30 (0.78, two.17) | |
Median unprocessed carmine meat intake | 0.9 | two.5 | 4.5 | vii.0 | 0.65 |
No. of events/no. of participants | 30/324 | 38/371 | 26/296 | 33/303 | |
Total person-years | 618 | 746 | 612 | 634 | |
Model 1 | ane.0 (ref) | 1.12 (0.69, 1.81) | 0.89 (0.52, 1.53) | 1.02 (0.threescore, ane.76) | |
Model 2 | 1.0 (ref) | 1.09 (0.67, 1.77) | 0.80 (0.44, 1.43) | 0.95 (0.55, one.66) | |
Median fish intake | 0.4 | i.three | ane.9 | 4.iii | 0.46 |
No. of events/no. of participants | 36/348 | 21/275 | 34/324 | 36/347 | |
Total person-years | 750 | 551 | 654 | 655 | |
Model 1 | one.0 (ref) | 0.80 (0.47, i.38) | 1.17 (0.73, i.88) | 1.23 (0.77, 1.97) | |
Model ii | 1.0 (ref) | 0.78 (0.45, 1.37) | one.07 (0.65, 1.73) | ane.13 (0.70, one.84) | |
Median poultry intake | ane.0 | two.0 | iii.0 | 5.5 | 0.17 |
No. of events/no. of participants | 33/380 | 24/224 | 35/344 | 35/346 | |
Total person-years | 782 | 474 | 694 | 660 | |
Model 1 | 1.0 (ref) | 1.36 (0.79, ii.31) | 1.29 (0.80, 2.x) | 1.42 (0.85, two.37) | |
Model 2 | ane.0 (ref) | 1.51 (0.87, 2.61) | 1.29 (0.78, ii.13) | i.55 (0.91, 2.66) | |
Median egg intake | 0.4 | 1.0 | 3.0 | five.v | 0.05 |
No. of events/no. of participants | 24/319 | 27/267 | 51/532 | 25/176 | |
Full person-years | 631 | 548 | 1084 | 347 | |
Model one | 1.0 (ref) | 1.30 (0.75, two.26) | 1.21 (0.74, 1.97) | 2.07 (1.xvi, 3.seventy) | |
Model ii | 1.0 (ref) | 1.17 (0.66, 2.07) | 1.06 (0.63, one.77) | 2.02 (1.10, three.72) |
To further explore the borderline significant association for poultry, nosotros analyzed poultry with and without skin separately ( Table four ). Consumption of skinless poultry was not associated with risk of prostate cancer progression. In contrast, men in the highest tertile of poultry with skin had more than a doubling in adventure of prostate cancer progression compared with men in the lowest tertile after adjustment for sociodemographic factors, clinical characteristics, and skinless poultry. Furthermore, at that place was evidence of a strong linear trend (HR: two.26; 95% CI: 1.36, iii.76, P for trend = 0.003).
TABLE 4
Tertile of intake | ||||
1 | two | 3 | P for trend ii | |
Median poultry with skin intake | 0.0 | one.0 | 3.0 | 0.003 |
No. of events/no. of participants | 48/584 | 46/473 | 33/237 | |
Total person-years | 1183 | 980 | 447 | |
Model ane three | ane.0 (ref) 4 | 1.19 (0.78, 1.84) | two.23 (1.39, three.59) | |
Model 2 v 6 | 1.0 (ref) | 1.22 (0.78, 1.92) | 2.26 (1.36, 3.76) | |
Median skinless poultry intake | 0.four | ane.0 | iii.0 | 0.87 |
No. of events/no. of participants | 35/344 | 42/391 | 50/559 | |
Total person-years | 691 | 804 | 1115 | |
Model i | 1.0 (ref) | ane.27 (0.fourscore, one.99) | ane.03 (0.64, i.63) | |
Model ii | i.0 (ref) | one.53 (0.95, 2.48) | 1.20 (0.73, 1.96) |
Adjustment for saturated fat did not materially modify the effect estimates for poultry with skin, skinless poultry, fish, or eggs. The point estimates for the comparison of extreme quartiles for processed and unprocessed scarlet meat decreased later adjustment for saturated fat, but remained statistically nonsignificant; the HR for candy red meat was ane.17 (95% CI: 0.68, 2.01) and for unprocessed carmine meat was 0.79 (95% CI: 0.41, 1.98).
We observed an interaction between prognostic take chances, total poultry, and risk of prostate cancer progression. Greater poultry intake was associated with increased risk of progression amid men with high prognostic adventure, only there was no association amongst men with depression/intermediate prognostic hazard (P for interaction = 0.003) ( Effigy 1 ). Men with loftier prognostic risk illness and in the highest quartile of poultry had a iv-fold increased take chances of progression compared with men with low/intermediate prognostic take a chance illness and depression poultry intake (60 minutes: iv.01; 95% CI: 1.82, 8.85). There was no evidence of a significant interaction betwixt prognostic risk and consumption of whatsoever other meat grouping or eggs. In addition, no interactions were observed betwixt BMI or fourth dimension from diagnosis to questionnaire and whatever of the meat groups or eggs.
Nosotros observed no pregnant associations between prognostic hazard and self-reported modify in diet subsequently diagnosis for any processed or unprocessed blood-red meat item, fish item, eggs, or poultry with skin. Men with high prognostic run a risk were somewhat less probable to report alter in consumption of skinless poultry after diagnosis compared with men with a low or intermediate prognostic risk. Approximately 8% of high-risk men reported eating more skinless poultry and none reported eating less compared with before their diagnosis of prostate cancer, whereas 10% of low-hazard men reported eating more skinless poultry and 2% of depression-risk men reported eating less compared with before their diagnosis (P value = 0.03).
In secondary analyses excluding the 38 men who initiated secondary handling of which we did non take biological evidence of recurrence (defined equally at to the lowest degree one posttreatment PSA ≥ 0.2 ng/mL after radical prostatectomy or at to the lowest degree one PSA ≥ 0.3 ng/mL higher up posttreatment nadir subsequently radiation or other treatment), the results for egg consumption remained positive but became nonsignificant (Hour for Q4 compared with Q1: 1.47; 95% CI: 0.72, 2.98), whereas the positive associations observed for total poultry (HR for Q4 compared with Q1: 1.80; 95% CI: 0.95, iii.41) and poultry with skin [HR for tertile (T) 3 compared with T1: 2.72; 95% CI: 1.51, 4.89) were strengthened.
Discussion
We observed no association between postdiagnostic consumption of processed or unprocessed ruddy meat, fish, or skinless poultry and risk of prostate cancer progression among 1294 men with a diagnosis of localized prostate cancer and followed for an average of two y. Even so, postdiagnostic consumption of poultry with skin and whole eggs were associated with 2-fold increases in risk of prostate cancer progression.
We acknowledge that our study had several limitations, including a short follow-up, a minor number of prostate cancer deaths or metastases, and a lack of prediagnostic dietary information. The Diet and Lifestyle substudy of CaPSURE has yet to accumulate many events of prostate cancer metastases or expiry. Thus, we included biochemical recurrence and initiation of secondary treatment in our outcome definition to ameliorate statistical power, just also because biochemical recurrence within two y of primary treatment is highly predictive of prostate cancer metastases and death, and secondary treatment is administered to patients with biochemical or clinical evidence of recurrence (23, 24, xxx–32). This outcome is appropriate in our study population because watchful waiting was rare (due north = 47); only half dozen (four.7%) of our events occurred in watchful waiters, and the exclusion of all watchful waiters did non materially change our results. In addition, our results did not change after we excluded men who initiated the secondary treatment of which we had no biological evidence of recurrence, which suggested that anxiety after prostate cancer diagnosis did not confound our observed associations.
Men were recruited into our report subsequently diagnosis of prostate cancer, so we were unable to collect prediagnostic dietary data. Every bit a effect, we could non examine the association betwixt these items and risk of prostate cancer. Nearly of the previous studies that examined poultry or eggs and gamble of prostate cancer reported no association (13). However, risk factors for incidence of total prostate cancer may differ from risk factors for advanced or fatal disease and thus it is plausible that poultry with peel and eggs may increase the risk of advanced prostate cancer or prostate cancer progression, only are non associated with risk of total prostate cancer (33). It is difficult to distinguish factors that affect initiation of aggressive prostate cancer from factors that bear on progression of the disease in epidemiologic studies. However, because the v-y survival of men with advanced prostate cancer is just 35%, it is important to identify modifiable factors that may prevent either the occurrence of advanced prostate cancer or its progression.
We are enlightened of simply one prior study of postdiagnostic consumption of whole foods and chance of prostate cancer progression. Our collaborative group examined the postdiagnostic intake of grains, vegetables, fruit, red meat, milk, fish, lycopersicon esculentum sauce, and fresh tomato products and prostate cancer progression among 1202 men with localized or regional prostate cancer in the Health Professionals Follow-Up Written report. In that study, red meat was not associated with the take chances of prostate cancer progression, and fish was inversely associated with take a chance of progression (17).
Our results for processed and unprocessed red meat are consistent with the prior study. However, we did not detect an association between fish intake and risk of prostate cancer progression. 2 cohort studies have reported an inverse association betwixt fish intake and advanced or metastatic prostate cancer and another reported an inverse clan between fish intake and prostate cancer mortality (ix, x, 12). The inconsistent results may reflect unmeasured genetic differences in the populations or variation in the type and corporeality of fish consumed. For example, Hedelin et al (34) reported an interaction between salmon-type fish and a variant in the COX-ii gene (rs5275: +6365 T/C) where, amid men with the variant allele, consuming salmon-type fish more than once per week was associated with a 72% decreased risk of prostate cancer compared with men who never consumed salmon-type fish, simply no association was observed among men with the wild-type genotype.
Our analyses of poultry and eggs were exploratory, considering no studies accept examined the postdiagnostic intake of these items and chance of prostate cancer progression (11, 13). However, in 2007, an international panel (35) concluded at that place was a possible positive clan between total poultry and prostate cancer run a risk, and Michaud et al (6) reported a positive association between poultry with skin and metastatic prostate cancer but an inverse association betwixt skinless poultry and metastatic prostate cancer. Our results concur with these findings and, although nosotros cannot rule out risk or misreckoning, our results did non change afterward we controlled for known sociodemographic, dietary, or clinical risk factors for prostate cancer incidence or mortality, and we observed a significant linear trend for poultry with peel.
On the basis of previous literature, we hypothesized that meat items high in saturated fatty may increase the risk of prostate cancer progression. Still, saturated fatty from poultry with skin did not explain our observed association betwixt poultry with pare and prostate cancer progression. An alternative mechanism that may explain our ascertainment for poultry with skin is a loftier intake of heterocyclic amines.
Heterocyclic amines are mutagens present at much higher concentrations in well-done poultry than in other meats (36, 37). We had no information on meat-training methods, but poultry with skin may be more than probable to be broiled or grilled than skinless poultry, which results in higher concentrations of heterocyclic amines (37). Heterocyclic amines induce prostate, colon, and mammary adenocarcinomas in rats and have been shown to covalently demark and harm DNA in cultured man prostate tissue and principal prostate cells (38–42). In epidemiologic studies, consumption of cooked meats, particularly grilled meat, and heterocyclic amines accept been associated with an increased risk of prostate and other cancers, although a few studies reported no association (8, 43–49).
A plausible mechanism that may explain our observed clan betwixt eggs and prostate cancer progression is high dietary choline. Egg consumption is a determinant of plasma choline, and college plasma choline was recently reported to exist associated with a greater run a risk of prostate cancer (50, 51). Malignant prostate cells accept higher choline concentrations than do healthy cells, and choline kinase is overexpressed in prostate cancer (52–54). In improver, considering of the increased uptake of choline by progressing prostate tumors, radiolabeled choline is used to place early prostate cancer recurrence (55). No studies have examined dietary choline and prostate cancer risk or progression; withal, college dietary choline has been associated with an increased chance of colorectal adenoma in women (56).
The strengths of our study included our prospective design and our comprehensive clinical, dietary, and sociodemographic data. All of our clinical information was collected by certified urologists and included important hazard factors for prostate cancer progression, including Gleason sum at diagnosis, PSA at diagnosis, and treatment. We were also able to control for many known and potential take chances factors for prostate cancer progression, such as age, race, BMI, smoking, didactics, and physical activeness.
Overall, our results support the hypothesis that diet may influence the progression of prostate cancer among men with localized affliction. In particular, consumption of poultry with skin and eggs may exist associated with an increased risk of prostate cancer progression.
Acknowledgments
The authors' responsibilities were as follows—JMC and ELR: developed the analysis program; ELR and AP: analyzed the data; ELR: drafted the manuscript; MJS: provided significant consultation; and China, JMC, and JMB: designed the study, obtained funding, and collected the data. All authors critically reviewed the manuscript and approved its concluding version. None of the authors had whatever personal or financial conflicts of interest.
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