Posted by Larry Hoover on June 14, 2006, at 8:35:33
In reply to Re: Increase in AA is not trivial » Larry Hoover, posted by dessbee on June 14, 2006, at 5:09:37
> I disagree. DGLA is an inflammatory precursor as well. An increase in AA is NOT trivial since it will lead to more PGE2.
> Supplements of GLA increases side effects of omega-6 since we already get too much af these fatty acids in our food.You didn't complete the conditions upon which your assertion is true. It is true if and only if there is insufficient eicosapentaenoic acid present to shunt the DGLA into PGE1 (or whichever one it is....I think it's class one). There is a fork in the road, and you can block one road, just by adding more traffic (in the form of omega-3 fatty acids, which have substantially higher affinities at the desaturases). Without the traffic, you're right. With it, you're not.
Some people have a form of desaturase that has a higher affinity for omega-6. They have to be very careful to adjust their fatty acid intake to permit any omega-3 to make it through the system, or they develop schizophrenia. There are conditions that must be considered, that limit the conclusions that can be reached. All conclusions are conditional. All of them. The hard part is simplifying, without messing up the conclusion.
Against the background of arachidonate from our 30- to 60-fold increase in omega-6 intake over the last century (primarily linoleic acid), which also coincided with a general decrease in omega-3 intake, taking a few hundreds of miligrams of one specific omega-6 is not going to matter. Just one order of fries, man, and that GLA is just swamped. (We were better off eating fries cooked in beef tallow [as MacDonalds once did], than we are eating them cooked in vegetable shortenings.) We eat so much omega-6 fatty acids that most of it is shunted to energy anyway. Unfortunately, that also shunts omega-3 to energy (enzymes are stupid, after all....a substrate is a substrate, to them), instead of into eicosanoids (EPA) and cell-wall composition (DHA).
Adult humans do not convert alpha-linolenic acid to DHA. It's virtually zero. Infants do it remarkably well. Pre-term infants, even better. But we lose the capacity, as we mature. Roughly 70% is lost to respiration. Only a few percent makes it to EPA. DHA stores can actually fall, on high ALNA diets. There is a lot of wrong information, out there.
It's a balancing act. And you can modify the balances. You can change the conditions to completely invert your initial outcomes. You can change a negative into a positive.
It's like sodium. For some people, high sodium intake causes hypertension, which is a cardiac risk factor, of course. So, they developed a simplified rule, to limit sodium for everybody who has a heart condition. Wrong. Wrong simplification. More people die on sodium restricted diets than those on free choice sodium diets. You have to have the condition, sodium hyper-responsivity, for the sodium restriction to apply. Other people are hurt by sodium restriction. They are more likely to suffer fatal heart attacks. And, all that, after suffering through low sodium diets. Maybe that's what kills them, the loss of the simple joy of eating salty food. <that was a wry humour concept>
It's the generalization that I challenge. All conclusions are conditional. There are boundary conditions. You change the conditions, you change the conclusion.
Lar
poster:Larry Hoover
thread:646450
URL: http://www.dr-bob.org/babble/alter/20060601/msgs/656781.html