Re Cancer cause has been found.

Once upon a time, our fellow nick rambled on about "Re Cancer cause has been found.." Our champion
De-Medicalizing in sci.med.nutrition retorts, thusly ...

Quoted message said:

when in fact, all one needs to do is avoid free radical damaged food

nice fairy tale, nick!

Ha, ... Hah, Ha!

nick said:

Those scientists supplied a basic physiological mechanism. The Aspirin Foundation was playing it up
to sell more aspirin, presumably, when in fact, all one needs to do is avoid free radical damaged
food, or food that is very susceptible to free radical degradation in vivo, and eat plenty of foods
high in antioxidants that don't have a "down side," such as most fruit. If

Seems like you have never understood how cyclooxygenase works. The enzyme is there, active, but
normally lacks substrates and an initiator that activate it. Free radicals both induce release of
the substrate, arachidonic acid from cell membranes by inducing phospholipase A2, which release the
fatty acid in position 2 (mid position) which is normally a PUFA, and in occasions of lack of PUFa,
of MUFA. The free radicals also is the activator of COX I and II, so the free radicals also fires up
COX which produce in first part PGG which in turn is changed into PGH plus a free radical which has
a certain chance to react with a tyrosine group in the active site of the enzyme. When the free
radical reacts with the tyrosin group, the enzyme is damaged and is out of catalytic work. Over
time, either enzyme dies or the local source of substrates (which otherwise could be DHGLA (C20:3
omega-6) and EPA, plus linoleic acid may bind and inhibit and in some rare occasions may produce PG-
alike molecules which are even more potent than the eicosanoids and may even react with NO2 to
produce very harmful liponitroxides. Free radicals and also some antioxidants may react with the
free radical formed during the catalytic cycle and hinder the suicidal downregulation of the enzyme
which is the natural effect. One antioxidant which may play havoc in the system is uric acid which
may produce rather nasty end products during the reaction, alloxan, which is used experimentally in
rats to induce diabetes,

Aspirin then kills the enzyme by reacting with a certain aminoacid sidegroup and acetylate that one.
Then the enzyme is also killed and cannot any more produce prostaglandins, eg. PGE2 which is a
strong immune system repressor or other products, dependent on where the enzyme function. The use of
aspirine in thinning blood is a twosided sword. Giving in doses used in inflammation and head aches
destroyes all enzymes in blood platelets and these platelets are not able any more to be involved in
the clog process. Giving just small doses on the other hand may inactivate only fractions of the
platelets, and then it is a good thing because many of the platelets may form clots y if needed, but
they are far less susceptible to being activated when not needed and forming clots during other
kinds of stresses, like cell membranes being harmed by mechanical stress during circulation of blood
in blood vessels (not all places there are linear transport of blood, and when veins etc. is
turning, there may occur tiny cavitation effects, disturbing the membrane layers of cell lining the
vessels and then inducing PLA2 and lipoxygenases (the main free radical producer by making lipid
peroxides enzynatically, eg. the famous leukotrienes which is a specific class of arachidonate
lipoxides) which in turn activates cyclooxygenase.