Fat type intakes (saturated, unsaturated,...) are optimized variably on genetics.
Eicosanoids (prostaglandins, …) are variably balanced on diet based on genetics. Some people, disposed, ancestrally, towards eating fish, will probably have relative underactive D6D (since the need for transitioning plant fats wasn’t necessary) and a disposition for higher series 2 activity (since there was relatively little arachidonic acid in the diet, it was necessary to be hyper-responsive to it), presenting the scenario wherein modern diets of high arachidonic acid (land animals) and low EPA and DHA (fish) will lead to an overactivity, and lack of mitigation, of series 2 prostaglandins. Depending on D6D activity, this situation can be rectified by {either ALA (adequate D6D activity) or consumption of DHA and EPA} and consumption of oleic acid (monounsaturated) to decrease series 2 activity.
