Just a few days apart, two studies have recently come out further raising the alarm about certain oils and cancer—one in prostate cancer and the other in colon.
“I first became aware of the potential risk of seed oil at a scientific meeting about 30 years ago,” says William J. Aronson, MD, Department of Urology, David Geffen School of Medicine, University of California Los Angeles. He is the lead author of the prostate paper, which appears in the Journal of Clinical Oncology.
His latest study followed men with prostate cancer on active surveillance (AS) who took specific supplements. Such men are very interested in dietary changes or supplements to prevent progression of their disease. The team sought to determine whether a high omega-3, low omega-6 fatty acid diet with fish oil capsules (D + FO) decreases proliferation in prostate biopsies in men with prostate cancer on AS over, a one-year time period. Omega 6 is found in seed oil, which has been suspected of encouraging cancer growth.
“We believe that the beneficial mix is a high omega-3, low omega-6 fatty acid diet with fish oil capsules,” says Aronson. “And we have a marker of proliferation—Ki67.”
Ki-67 is a protein that is found only in cells that are dividing. A high Ki-67 proliferation index means many cells are dividing quickly and that the cancer is likely to grow and spread. In this study, 100 men with grade group 1 or 2 prostate cancer who elected AS were randomly assigned to the D + FO or a control group. Same-site prostate biopsies were obtained at baseline and one year. The primary end point was the change in Ki-67 index from baseline to one year from same-site biopsies compared between the groups.
The team found that the Ki-67 index decreased in the D + FO group by approximately 15% from baseline to one year and increased in the control group by approximately 24% from baseline to one year, resulting in a statistically significant difference in the change of Ki-67 index between the two groups.
The colon cancer cancer study was led by a team from University of South Florida Health, Tampa. It appeared in Gut and the lead author is Ramani Soundararajan, of the department of surgery at University of South Florida Health.
They performed liquid chromatography and tandem mass spectrometry (LC–MS/MS) untargeted analysis of 40 human colorectal (CRC) and normal paired samples and targeted, quantitative analysis of 81 human CRC and normal paired samples. They integrated analysis of lipidomics, quantitative reverse transcription-PCR, large scale gene expression, and spatial transcriptomics with public scRNASEQ data to characterize pattern, expression and cellular localization of genes that produce and modify lipid mediators.
They found that targeted, quantitative LC–MS/MS revealed a marked imbalance of pro-inflammatory mediators, with a dearth of resolving lipid mediators. In tumors, they observed saw prominent over-expression of arachidonic acid derivatives, the genes encoding their synthetic enzymes and receptors, but poor expression of genes producing pro-resolving synthetic enzymes and resultant lipoxins (LXA4, LXB4) and associated receptors. (Seed oils contain arachidonic acid.)
The authors believe their results indicate that CRC is the product of defective lipid class switching likely related to inadequate or ineffective levels of PGE2/PGD2.
“The old adage is true, you are what you eat,” says Aronson. “We just need to be sure what you should be eating.”
