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Case–control and prospective studies of dietary α-linolenic acid intake and prostate cancer risk: a meta-analysis
  1. Amanda J Carleton1,2,3,
  2. John L Sievenpiper1,2,4,
  3. Russell de Souza1,2,5,6,
  4. Gail McKeown-Eyssen2,7,
  5. David J A Jenkins1,2,3
  1. 1Clinical Nutrition and Risk Factor Modification Centre and Keenan Research Centre of the Li Ka Shing Knowledge Institute, St Michael's Hospital, Toronto, Ontario, Canada
  2. 2Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
  3. 3Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
  4. 4Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Toronto, Ontario, Canada
  5. 5Department of Nutrition, Harvard School of Public Health, Harvard University, Boston, Massachusetts, USA
  6. 6Department of Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Ontario, Canada
  7. 7Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada
  1. Correspondence to Dr Amanda J Carleton; amanda.carleton{at}


Objective α-Linolenic acid (ALA) is considered to be a cardioprotective nutrient; however, some epidemiological studies have suggested that dietary ALA intake increases the risk of prostate cancer. The main objective was to conduct a systematic review and meta-analysis of case–control and prospective studies investigating the association between dietary ALA intake and prostate cancer risk.

Design A systematic review and meta-analysis were conducted by searching MEDLINE and EMBASE for relevant prospective and case–control studies.

Included studies We included all prospective cohort, case–control, nested case-cohort and nested case–control studies that investigated the effect of dietary ALA intake on the incidence (or diagnosis) of prostate cancer and provided relative risk (RR), HR or OR estimates.

Primary outcome measure Data were pooled using the generic inverse variance method with a random effects model from studies that compared the highest ALA quantile with the lowest ALA quantile. Risk estimates were expressed as RR with 95% CIs. Heterogeneity was assessed by χ2 and quantified by I2.

Results Data from five prospective and seven case–control studies were pooled. The overall RR estimate showed ALA intake to be positively but non-significantly associated with prostate cancer risk (1.08 (0.90 to 1.29), p=0.40; I2=85%), but the interpretation was complicated by evidence of heterogeneity not explained by study design. A weak, non-significant protective effect of ALA intake on prostate cancer risk in the prospective studies became significant (0.91 (0.83 to 0.99), p=0.02) without evidence of heterogeneity (I2=8%, p=0.35) on removal of one study during sensitivity analyses.

Conclusions This analysis failed to confirm an association between dietary ALA intake and prostate cancer risk. Larger and longer observational and interventional studies are needed to define the role of ALA and prostate cancer.

  • Nutrition & Dietetics
  • Preventive Medicine

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