TC:

Don't try to reason with this character.  He appears to be a deluded
megalomaniac, if you haven't noticed already.  Let him eat his whole
wheat bread with safflower and fish oil spread all over it.  Then, it
won't be long before we never hear from him again.

For those who want to know what it really going on (at the molecular
level), a recent experimental study (as opposed to the
association/correlations ones that make all kinds of unreasonable
assumptions before they even start it) is right on point particularly
the statement:

"...endogenously produced [that is, it is produced in your body, by
your cells, because you ate omega 6s beyond a threshold amount]
8-iso-PGF(2a) during oxidant stress induces prostaglandin formation
presumbly through the classical cyclooxygenase-catalysed arachidonic
acid oxidation which might be inflammatory itself to the cells..."

Whole grains might indeed "mop up" some of the omega 6 PUFAs and remove
them from the body, as well as perhaps having antioxidant properties,
but simply avoiding omega 3 and 6 PUFAs to begin with makes the most
sense.  Then, you can just eat bread in moderation made with
unbleached, organic flour, and you don't have to worry about "fiber" of
any kind.

Free Radic Res. 2006 Mar;40(3):273-7.

F(2)-isoprostane induced prostaglandin formation in the rabbit.

Basu S.

Uppsala University, Section of Clinical Nutrition and Metabolism,
Department of Public Health and Caring Sciences, Faculty of Medicine,
Uppsala Science Park, Uppsala, SE, 751 85, Sweden.

F(2)-isoprostanes, non-enzymatic free radical mediated products of
arachidonic acid, have shown to form during various oxidant stress
status and have potent biological effects. This study investigates to
what extent 8-iso-PGF(2a) (a major F(2)-isoprostane), a bioactive
product of lipid peroxidation can modify endogenous prostaglandin F(2a)
(PGF(2a)) formation since prostaglandins are inflammatory as well as
potent vasoregulatory substances that modulate diverse important
physiological functions, and also form during acute and chronic
inflammation. An immediate appearance and disappearance of
8-iso-PGF(2a) was seen in both plasma and urine within a short interval
after i.v. administration of 43 microg/kg of 8-iso-PGF(2a) to the
rabbits. A successive but differential formation of PGF(2a) resulted in
a rapid and pulsatile increase of plasma 15-keto-dihydro-PGF(2a), a
major metabolite of primary PGF(2a). Later, this compound was excreted
efficiently as intact compound into the urine during the 3 h of
experiment. A 8-fold increase of PGF(2a) metabolite in plasma at 10 min
and 12-fold increase in the urine at 30-60 after the i.v.
administration of 8-iso-PGF(2a) was observed which continued throughout
the 3 h of experiment. This observation suggests that pharmacologically
administered or endogenously produced 8-iso-PGF(2a) during oxidant
stress induces prostaglandin formation presumbly through the classical
cyclooxygenase-catalysed arachidonic acid oxidation which might be
inflammatory itself to the cells and exerts further vasoconstrictive
effects.