Comprehensive Investigation on Associations between Dietary Intake and Blood Levels of Fatty Acids and Colorectal Cancer Risk

Abstract: Background: Increasing studies have discovered that different fatty acids (FAs) are linked to colorectal cancer (CRC) risk.

Methods: We systematically searched Embase and Med-line databases to identify eligible studies that examined the associations of different types of FAs with CRC risk. The effect estimates and their 95% confidence intervals (CIs) were pooled using a random-effects model. Subgroup and sensitivity analyses were performed to examine the ro-bustness of study findings.

Results: This study evaluated the associations of 28 dietary and 18 blood FAs with CRC risk by summarizing the most updated evidence from 54 observational and 4 Mendelian Randomization (MR) studies. The present findings suggested that high dietary in-take of eicosapentaenoic acid (EPA), docosahexanoic acid (DHA), and docosapentaenoic acid (DPA) are related to low risk of CRC, while n-6/n-3 PUFA ratio and trans-FA are related to high risk of CRC. The summary of all cohort studies found that high intake of SFA and DHA was a protective factor for CRC, and high intake of n-6/n-3 PUFA ratio was a risk factor for CRC. In the subgroup analysis of cancer subsites, we found that dietary intake of linoleic acid (LA) and trans-FA are risk factors, while DPA is a protective factor for colon cancer. More DHA intake was associated with lower rectal cancer risk, while higher dietary n-6/n-3PUFA ratio was associated with higher rectal cancer risk. Meta-analysis of blood FA levels showed a significant reverse as-sociation between blood pentadecanoic acid and CRC risk, whilst other blood FAs showed no significant association with CRC risk. All included MR studies showed that high plasma arachi-donic acid (AA) is associated with increased CRC risk.

Conclusions: At present, the evidence about dietary intake and blood levels of FAs and CRC risk is less consistent. Future studies are needed to investigate how the metabolism of FAs contributes to CRC development.