Corn oil is actually worse because it has much more linoleic acid, the only precursor to the prostaglandins.
The old studies on high‐fat diets in rats, dating back to the '40s, had shown a high fat diet to promote cancer. Later on, in the '70s, it had been shown that some fats were far more carcinogenic than others. The most carcinogenic fatty acid was always corn oil.
And then later, in the '80s, review articles from all these fat‐feeding rat studies had teased‐out one important finding: linoleic acid content! While it's common to separate fatty acids into two groups, saturated and unsaturated, this is a simplification which hides important details. Only arachidonic acid can become prostaglandins, and arachidonic acid is exclusively made from linoleic acid. When arachidonic acid is concentrated on the cell membrane, you have potential for 'inflammation' and cancer.
The enzyme phospholipase A₂ cleaves arachidonic acid from a phospholipid on the cell membrane. This is a cool enzyme, and it can do this in vitro. This enzyme can be shown to work using simple micelles—or artificial lipid droplets in water—constructed of phosphotidylcholine, with arachidonic acid at the sn‐2 position or course. This enzyme has an affinity for the lipid membrane and can catalyze the cleavage of the arachidonic acid–phospholipid bond.
Released arachidonic acid then diffuses towards cyclooxygenase, which adds O₂ to the lipid forming the endoperoxide ring characteristic of prostaglandin H. This is then isomerized to either prostaglandin D₂ or prostaglandin E₂. These have opposing functions, to a degree, as prostaglandin D₂ usually constricts the blood vessels while prostaglandin E₂ always relaxes them.
But they have hormonal functions to, besides those mediated through their G protein‐coupled receptors on microtubules. The PPAR series of nuclear receptors can bind prostaglandins, and then induce transcription of enzymes and proteins.
But there is another twist, since the entire process can be mitigated by competing fatty acids. Oleic and eicosapentaenoic acids have been shown to inhibit prostaglandin production by: (1) Displacing it from the cell membrane, and (2) Competing with it for the cyclooxygenase enzyme. This is why ω−3 fatty acids are considered 'protective.'
But omega−3 fatty acids cannot be said to be 'protective' against spontaneous oxidation or lipofuscin. In fact, some of them are even more prone to oxidation since they can have upwards of six double‐bonds. So between corn oil and fish oil you are presented with a dilemma: Either you can have the growth promoting, proliferative, and carcinogenic corn oil . . . or you can have the more unstable yet relatively non‐proliferative fish oil. If a person had cancer, they'd probably have to choose the fish oil; but if a person was underweight and taking iron supplements for some reason, the more stable corn oil could be a better choice.
But I would think the IQ point difference could have been influenced more by the vitamins in the fish oil. This oil is naturally rich in vitamin A, but it also has significant amounts of vitamin D. However, it is often deodorized—a process which largely removes these vitamins. Sometimes they are added back in, but the concentrations are always somewhat unnatural (vitamin A‐heavy). Vitamin A is powerful lipid hormone which can effect nearly everything. Active vitamin A, or retinoic acid, has two nuclear receptors which double as transcription factors. Upon binding retinoic acid, these receptors cumulatively transcribe DNA for thousands of genes.
It would be nice to see a study controlling for vitamin A, also having a coconut oil group.
Actually, a much more recent study kept calling corn oil a known "tumor promoter" and used glycine to block its effects. So, apparently in some scientific circles the truth is well-known.
PUFA are carcinogenic, dietary glycine blocks their effect