The Rapeseed Association of Canada took the opportunity to rename the plant, and “Can” for Canada, plus “ola” for oil, was born. Producers are still keen to leave the rapeseed designation behind, hence their claim that this GM-version is a distinct type of plant. Essentially, it is a very comprehensive marketing campaign designed to confuse and lead the public to a foregone conclusion.
With more than 90% of U.S. crops and upwards of 80% of Canadian canola derived from genetically-engineered seeds, it’s almost certain that your bottle of canola oil comes from plants contaminated with chemical herbicides. Because processing removes the genetically-modified protein from the finished oils, producers consider it the same as conventional oil, believing this production process removes all potential for harm. It is therefore marketed as being 100% safe for unlimited human consumption. But as the latest medical science points out, this oil is far from being a healthy choice for human brains and bodies.
Canola oil is often promoted as a low-cost alternative to olive oil, possessing the same health benefits. It’s even promoted as having a mere 7% saturated fat, compared to olive oil’s 15%. But what does science say about the healthfulness of canola? Until recent years, no data were available on the effect of canola oil intake in relation to increasingly common diseases, like Alzheimer’s disease. Canola oil had never been examined as a causal factor in the sixteen-fold increase in deaths from Alzheimer’s reported in 1991: a total of 14,112, up from just 857 deaths reported in 1979.
In December 2017, researchers from Alzheimer’s Center at Temple University investigated the effect of daily consumption of canola oil on mice whose brains had developed both plaques and tangles, common brain characteristics for Alzheimer’s patients. Mice in the control group received a typical diet, while mice in the experimental group were fed a diet supplemented with canola oil for a period of 6 months. At the beginning of the study, mice had the same body weight. They were put through three different tests involving memory functions and conditioning, such as mazes. Ability to navigate these environments demonstrated measurable brain function and emotional stimulation..
(A&B) The mtDNA level in PARP1+/- chagasic mice. Mice (WT and PARP1+/-) were infected with T. cruzi and monitored at 150 days’ post-infection. Representative gel images (A, n = 3 mice/group) show myocardial levels of 10 kb mtDNA and short 177-bp mtDNA and 96-bp nuDNA (GAPDH) fragments as controls. PCR amplification was performed for 28 cycles. Densitometry analysis was performed on PCR gels representing n? 6 mice/group, and density of the 10 kb mtDNA band, normalized against mtDNA and nuDNA fragments, is presented in B.a&b. (C-H) Effect of PARP1 inhibitor on cardiomyocytes infected with T. cruzi. Cardiac myocytes were infected with T. cruzi in presence or absence of PJ34 for 24 h. RT-qPCR was employed to evaluate the mRNA level for PARP1 and several components of the POLG replisome machinery, and data were normalized to GAPDH mRNA. (I-K) Cardiomyocytes were incubated for 24 with Tc in presence and absence of PJ34. ROS release was measured by an amplex red assay (I). MitoSOX red fluorescence detects mitochondrial O2•? level (J). Ratio of fluorescence intensity of J-monomers (green) to J-aggregates (red) indicates mitochondrial depolarization (K). Data in C-K were acquired by using three biological replicates (duplicate analysis per sample). Data in all bar graphs are plotted as mean value ± SEM, and statistical significance are marked as *WT.Tc vs. WT, and #WT.Tc vs. genetically-modified/infected or infected/PJ34-treated (#p<0.05, ***,###p<0.001).