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Table 4 Summary of observational studies on the association between ARA and risk of prostate cancer

From: Arachidonic acid and cancer risk: a systematic review of observational studies

References Study Subjects Exposure Assessment Prostate cancer assessment (diagnosis) Adjustment for potential confounders Assessment of reporting quality * Main findings
Intergroup comparison   P or Ptrend
Study design: cohort study
Exposure assessment: dietary intake
Leitzmann et al. 2004 [67] HPFS, USA, 1986-2000, prospective cohort design (14 years follow-up) 47,866 health professionals aged 40-65, no prior history of cancer Semiquantitative FFQ, 131 items, validated against 2 x 1-week DR Self-reported physician diagnosis supplemented by medical record and pathology report Age, time period, race, family history of prostate cancer, history of type 2 DM and vasectomy, BMI, height, smoking status, physical activity, total energy intake, % of energy from protein intake, monounsaturated fat intake, saturated fat intake and trans unsaturated fat intake, calcium intake, supplemental vitamin E and lycopene 21 Dietary ARA intake, %energy, quintile RR(95% CI) Ptrend
Q1: <0.028 1.00 0.44
Q2: 0.028-0.035 1.06(0.94-1.19)
Q3: 0.036-0.041 1.04(0.92-1.18)
Q4: 0.042-0.049 1.02(0.89-1.16)
Q5: >0.049 1.08(0.94-1.25)
Study design: nested case-control study
Exposure assessment: dietary intake
Männistö et al. 2003 [68] ATBC study, Finland, 1985-1993, nested case-control design (5-8 years follow-up) 198 prostate cancer patients, 198 controls (free of prostate cancer) matched by age, trial supplementation group Self-administered dietary questionnaire, 276 items, validated against 12 x 2-day DR Finnish Cancer Registry and Register of Causes of Death Resident area, educational level, BMI, alcohol intake, smoking period 23 Dietary ARA intake, g/day, median OR(95%CI) Ptrend
Q1: 0.04 1.00 0.23
Q2: 0.06 0.89(0.52-1.54)
Q3: 0.07 1.10(0.64-1.90)
Q4: 0.10 1.31(0.77-2.21)
Schuurman et al. 1999 [69] NLCS, Netherlands, 1986-1992 (6.3 years follow-up), case-cohort design 642 primary prostate cancer patients from entire cohort, 1,525 subcohort members (selection criteria not shown) aged 55-69 at baseline, without prevalent cancer other than skin cancer, matching not indicated Semiquantitative FFQ, 150 items, validated against 3 x 3-day DR All regional cancer registries and Dutch national database of pathology reports Age, family history of prostate carcinoma, socioeconomic status, total energy intake, total energy-adjusted fat intake 23 Dietary ARA intake, g/day, quintile, median RR(95%CI) Ptrend
Q1: 0.06 1.00 0.30
Q2: 0.09 1.21(0.88-1.66)
Q3: 0.11 1.37(1.00-1.87)
Q4: 0.13 1.11(0.80-1.54)
Q5: 0.17 1.20(0.87-1.66)
Exposure assessment: blood ARA level
Crowe et al. 2008 [70] EPIC study, Denmark, Germany, Greece, Italy, Netherlands, Spain, Sweden, UK, 1992-2000, nested case-cohort design 962 prostate cancer patients, 1,061 controls without prevalent cancer other than NMSC, 1 case matched with 1-2 control(s) by study center, age, time of blood sampling, time between blood sampling and last consumption of food or drink Plasma phospholipids, GC analysis, precision indicated Regional or national cancer registries or combination of health insurance records, cancer and pathology registries and self-report BMI, smoking status, alcohol intake, educational level, marital status, physical activity 26 ARA composition mol%, quintile RR(95%CI) Ptrend
Q1: 4.40–7.93 1.00 0.419
Q2: 7.93–8.89 1.28(0.96-1.70)
Q3: 8.90–9.86 1.17(0.88-1.56)
Q4: 9.86–10.98 0.81(0.60-1.10)
Q5: 10.99–19.14 0.91(0.65-1.25)
Chavarro et al. 2007 [71] PHS, USA, 1982-1995, nested case-control design within a randomized, double-blind, placebo-controlled factorial aspirin and beta-carotene trial (13 years follow-up) 476 prostate cancer patients, 476 controls, male physicians without history of cancer except NMSC, 1 case matched with 1 control by age, smoking status, with consideration for trial intervention Whole blood fatty acids, GC analysis blinded to case-control status, precision indicated Self-report, combined with review of hospital records and pathology reports Age, smoking status, length of follow-up 22 ARA concentration (%,), quintile, median OR(95%CI) Ptrend
Q1: 7.9 1.00 0.98
Q2: 9.3 1.22(0.82-1.81)
Q3: 10.1 1.05(0.70-1.57)
Q4: 10.9 0.98(0.66-1.46)
Q5: 12.3 1.09(0.72-1.64)
Männistö et al. 2003 [68] ATBC study, Finland, 1985-1993, nested case-control design (5-8 years follow-up) 198 prostate cancer patients, 198 controls (free of prostate cancer) matched by age, trial supplementation group Serum cholesterol ester fatty acids, GC analysis, precision indicated Finnish Cancer Registry and Register of Causes of Death Resident area, educational level, BMI, alcohol intake, smoking period 23 ARA composition %, quartile, median OR(95%CI) Ptrend
Q1: 3.96 1.00 0.34
Q2: 4.55 1.05(0.60-1.84)
Q3: 5.09 0.94(0.54-1.64)
Q4: 5.89 1.39(0.79-2.44)
Harvei et al. 1997 [72] Janus serum bank, Norway, 1973-1994, nested case-control design 141 prostate cancer patients, 282 controls (eligibility criteria not shown), 1 case matched with 2 controls by age, date of blood sampling, resident area Serum phospholipids, GC analysis, blinded to case-control status, precision not indicated Cancer Registry and Statistics Norway None 14 ARA concentration mg/l, quartile, upper limit OR(95%CI) Ptrend
Q1: 4.86 1.0 0.6
Q2: 5.68 1.1(0.6-1.9)
Q3: 6.68 1.2(0.7-2.1)
Q4: >6.68 0.8(0.4-1.5)
Gann et al. 1994 [73] PHS, USA, 1982-1988, nested case-control design within a randomized, double-blind, placebo-controlled factorial aspirin and beta-carotene trial (6 years follow-up) 120 prostate cancer patients, 120 controls, male physicians without history of cancer except NMSC, 1 case matched with 1 control by age, smoking status without regard to trial intervention Plasma cholesterol ester fatty acids, GC analysis blinded to case-control status, precision indicated Self-report, combined with review of medical records None 19 ARA composition of plasma cholesterol estel %, quartile OR Ptrend
Q1 1.00 0.76
Q2 1.81
Q3 1.00
Q4 1.36(vs Q1 95% CI: 0.63-2.90)
Study design: case-control study (temporal relationship among exposure and outcome is unclear)
Exposure assessment: dietary intake
Hodge et al. 2004 [74] Survey, Australia, 1994-1997, case-control design 858 prostate cancer patients aged <70, 905 controls matched by age Melbourne FFQ, 121 items, validated against 2 x 4-day WFR Not shown Age at selection, study center, calendar year, family history of prostate cancer, country of birth, socioeconomic status 18 Dietary ARA intake, g/day, quintile OR(95%CI) Ptrend
Q1: <0.028 1.0 0.6
Q2: 0.028-0.036 1.2(0.8-1.6)
Q3: 0.037-0.046 1.2(0.8-1.6)
Q4: 0.047-0.059 1.0(0.7-1.3)
Q5: ≥0.06 1.0(0.7-1.4)
Exposure assessment: blood ARA level
Ukori et al. 2010 [75] Survey, USA and Nigeria, case-control design 48 African American and 66 Nigerian prostate cancer patients, 96 African American and 226 Nigerian controls, aged ≥40, without any cancer history other than skin cancer, matching not indicated Plasma fatty acids (fasting blood), GC analysis, precision not indicated Abnormal DRE and/or abnormal PSA (>4ng/ml) with histological diagnosis Age, educational level, family history of prostate cancer, WHR 14 ARA concentration μg/ml, quartile American African: OR(95%CI) Ptrend
Q1 vs Q4 American African: American African:
Nigerian: 0.3(0.08-1.11)  
Q1 vs Q4 Nigerian: <0.05
0.75(0.32-1.74) Nigerian:
Not significant
Ukori et al. 2009 [76] Survey, Nigeria, case-control design 66 prostate cancer patients, 226 controls, aged ≥40, matching not indicated (same population as Nigerian participants of Ukori et al. 2010) Plasma fatty acids (fasting blood), GC analysis, precision not indicated Abnormal DRE and/or abnormal PSA (>4ng/ml) with histological diagnosis Age, educational level, family history of prostate cancer, WHR 11 ARA concentration μg/ml, quartile OR(95%CI) Ptrend
Q1 1.00 0.06
Q2 2.59(0.85-7.86)
Q3 1.93(0.73-5.14)
Q4 0.75(0.32-1.74)
Newcomer et al. 2001 [77] Survey, USA, case-control design 67 prostate cancer patients, 156 population-based controls, 1 case matched with about 2 controls by age distribution Erythrocyte fatty acids, GC analysis blinded to case-control status, precision indicated Not shown Age 23 ARA composition weight%, quartile OR(95%CI) Ptrend
Q1: ≤13.25 1.0 0.88
Q2: 13.26-14.12 1.6(0.7-3.7)
Q3: 14.13-14.90 1.6(0.7-3.5)
Q4: ≥14.91 0.9(0.4-2.3)
Yang et al. 1999 [78] Survey, Korea 19 prostate cancer patients, 24 benign prostatic hyperplasia patients, 21 normal controls, matched by age, demographics Serum fatty acids, GC-MS analysis, precision not indicated Not shown None 4 ARA composition%, mean (SD) ARA composition%, mean(SD) P
Cancer: Normal control: Not significant
0.77(0.31) 1.15(0.45)
Benign:
0.95(0.16)
Study design: cross-sectional study
Exposure assessment: blood ARA level
Faas et al. 2003 [79] Survey, USA, 1995-1998 Prostate cancer patients, benign prostate disease patients Erythrocyte and plasma phospholipids, GC analysis, precision not indicated Pathology reports None 10 Erythrocyte ARA composition%, mean(SEM) Erythrocyte ARA composition%, mean(SEM) P
Malignant: Benign: Erythrocyte:
16.33(0.28) 16.68(0.25) Not significant
Plasma ARA composition%, mean(SEM) Plasma ARA composition%, mean(SEM) Plasma:
Malignant: Benign: Not significant
12.60(0.27) 13.03(0.29)
Hietanen et al. 1994 [46] Survey, UK, cross-sectional design 10 prostate cancer patients aged 64-85, controls, matched by age, sex, smoking status Erythrocyte phospholipids (fasting blood), GC analysis, precision not indicated Not shown None 8 ARA composition%, mean(SD) ARA composition%, mean(SD) P
Case: Control: Not significant
17.8(1.3) 18.6(1.3)
Chaudry et al. 1991 [80] Survey, UK 20 patients admitted for prostatic surgery (10 malignant, 10 benign) Plasma phospholipids (fasting blood), GC analysis, precision not indicated Histological diagnosis None 6 ARA composition%, median(IQR) ARA composition%, median(IQR) P
Malignant: Benign: Not significant
8.93(1.84) 8.78(2.03)
Exposure assessment: tissue ARA level
Faas et al. 2003 [79] Survey, USA, 1995-1998 Prostate cancer patients, benign prostate disease patients Prostate tissue phospholipids, GC analysis, precision not indicated Pathology reports None 10 ARA composition%, mean(SEM) ARA composition%, mean(SEM) P
Malignant: Benign: <0.001
15.20(0.33) 16.99(0.29)
Mamalakis et al. 2002 [81] Survey, Greece, 1997-1999 36 prostate cancer patients, 35 benign prostate hyperplasia patients Gluteal adipose tissue and prostate tissue fatty acids, GC analysis, precision not indicated DRE, serum PSA, transrectal ultrasound, prostate biopsy None 12 Gluteal adipose tissue ARA composition%, mean(SD) Gluteal adipose tissue ARA composition%, mean(SD) P
Malignant: Benign: Gluteal adipose tissue:
0.28(0.12) 0.25(0.14) Not significant
Prostate tissue ARA composition%, mean(SD) Prostate tissue ARA composition%, mean(SD)  
Malignant: Benign: Prostate tissue:
5.99(3.65) 10.71(2.69) <0.001
Chaudry et al. 1991 [80] Survey, UK 20 patients admitted for prostatic surgery (10 malignant, 10 benign) Prostate tissue phospholipids, GC analysis, precision not indicated Histological diagnosis None 6 ARA composition%, median(IQR) ARA composition%, median(IQR) P
Malignant: Benign:  
11.33(4.12) 15.55(2.54) 0.002
  1. ARA Arachidonic acid, ATBC Study: Alpha-tocopherol. Beta-carotene cancer prevention study, BMI Body mass index, DM Diabetes mellitus, DR Diet record, DRE Digital rectal examination, EPIC European prospective investigation into cancer and nutrition, FFQ Food frequency questionnaire, GC Gas chromatography, HPFS Health professionals follow-up study, IQR Interquartile range, NLCS Netherlands cohort study on diet and cancer, NMSC Non-melanoma skin cancer, OR Odds ratio, PHS Physician's health study, PSA Serum level of prostate specific antigen, RR Relative risk, UK United Kingdom, USA United States of America, USDA United states Department of Agriculture, WFR Weighed food record, WHR Waist-to-hip ratio.
  2. *Result of the critical evaluation carried out using the STROBE tool.