Induction of mitochondrial nitrative damage and cardiac dysfunction by chronic provision of dietary ω-6 polyunsaturated fatty acids
Introduction
I think intuitively we all know that seed oils are bad for us. Something that was created at most 70 years ago should not be part of the human diet. With that being said, I wanted to go out and prove that seed oils are in fact bad. Fortunately for me, there is actually a lot of research to back this up.
This first study I looked at titled “Induction of mitochondrial nitrative damage and cardiac dysfunction by chronic provision of dietary ω-6 polyunsaturated fatty acids” was conducted by Ghosh and colleagues. They took two groups of mice and put one on a high PUFA diet (HP group) and gave the second group a normal mice diet (LP group). This was done for 4 weeks, and then the researchers dissected the mice and got us the results.
Major Points
The first takeaway (maybe not so much a takeaway since this is expected), is that the cardiac PUFA content in free form in the HP group was significantly higher than the LP group (which is the main variable the researchers changed. The Omega 3 (DHA, and EPA) also increased in the HP group, however the omega-6’s increased 3x as much.
The next major difference between the two groups was nitrative stress. There is ROS (reactive oxygen species, but we also have RNS (reactive nitrogen species). They function in similar ways. Under pathological conditions, excess NO (nitric oxide) is generated by NOS (nitric oxide synthase). NO when combined with superoxide can form the most damaging oxidant, peroxy-nitrite (ONOO-). ONOO- nitrates tyrosine residues of proteins to produce nitrotyrosine. This molecule was significantly elevated in the HP group. The reason this is important is because peroxy-nitrite can oxidize mitochondrial DNA (mDNA). On top of this, the researchers found a significant decrease in superoxide dismutase (SOD)- which is one of the strongest antioxidants made in our body (along with glutathione).
Probably related to that- researchers found a decrease in gene expression associated with energy production specifically NADH dehydrogenase subunit 1 (ND-1) and ATPase 6- this is associated with decreased mitochondrial respiration.
Lastly, the researchers found decreased work capacity at increased workloads in the HP group compared to the LP group- although it was similar when less work was performed.
Summary:
At least in rats (although I would argue in humans as well). There is an association between increased PUFA consumption and decreased work capacity, increased ROS and RNS, increased mitochondrial damage, decrease in cardiolipin and decreased energy production in mitochondria.
PUFA content in free form in HP vs LP group
Cardiolipin in high low PUFA vs high PUFA groups
Nitrative production measured iNOS