Open AccessDietary Trans Fatty Acid Intake in Relation to Cancer Risk: A Systematic Review
Author(s) -
Nathalie Michels,
Karen van der Meulen,
Isabelle Huybrechts
Publication year - 2018
Publication title -
journal of global oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.002
H-Index - 17
ISSN - 2378-9506
DOI - 10.1200/jgo.18.45900
Subject(s) - medicine , cancer , pancreatic cancer , breast cancer , prostate cancer , colorectal cancer , oncology , fatty acid , gastroenterology , gynecology , biochemistry , biology
Background: A western-type diet is probably the key modifiable risk factor toward cancer. Ultra-processed foods may contain trans fatty acids produced during partial oil hydrogenation. Aim: Harmful cardiovascular effects of trans fatty acids are already proven, but the link with cancer risk has not been summarized yet. Methods: The online electronic databases PubMed (n=375 articles) and Embase (n=122 articles) were used to find observational studies on the intake of trans fatty acids as predictor of neoplasms. The full-text of 78 articles was read by two independent researchers, after a first elimination based on abstract, and eventually 24 articles were included in this review. Results: In total, 7 cancer types have been researched in cohort and case-control studies investigating associations between trans fatty acid intakes and cancer risk: breast cancer (n=6), colorectal cancer (n=9), mouth/pharynx/esophagus cancer (n=3), non-Hodgkin lymphoma (NHL, n=4), ovarian cancer (n=5), pancreatic cancer (n=3) and prostate cancer (n=6). Concerning total trans fatty acid intake, the studies on NHL and oral/pharynx/esophagus cancer univocally showed a positive association, while the ones on pancreatic cancer showed no significant association and the other cancers had contradictory results. Some studied subtypes of trans fatty acids: C16:1 and C18:2 but not C18:1 were related to breast cancer; C16:1 but not C18:1 or C18:2 were related to pancreatic cancer; while results for colorectal and prostate cancer were contradictory. For C18:1, even the place of the double bound can change the relation with prostate cancer. Vulnerability factors were genetics (for prostate cancer), ethnicity (Caucasian more at risk for prostate or colorectal cancer), menopause (for breast cancer), high age (for colon and prostate cancer) and high BMI (for colon cancer). Conclusion: This systematic review suggests potential harmful effects of high consumptions of trans fatty acids through increased cancer risks, with most evidence available for NHL and oral/pharynx/esophagus cancer. Underlying pathways are not fully known, but chronic inflammation and oxidative stress possibly play a role. Future studies investigating associations between trans fat intakes and cancer risk should apply higher methodological quality (eg adjusting for confounders and using biomarkers of intake). For targeted prevention strategies, studies should examine which trans fatty acid subtypes are more carcinogenic and what populations are at highest risk.