I read some of Modern Nutrition in Health and Disease (9th Edition), which Monty/HSWC has mentioned in discussions previously. Here is some information about EFA deficiency.
Pages 88-92. They say that 18:2 omega-6 at just 1-2% of calories will prevent symptoms of EFAD in rats. They claim the signs of EFAD are "reduced growth rates", "scaly dermatitis", "increased loss of water by a change of skin permeability", male/female infertilty, and "depressed inflammatory responses."
(Comment: I don't see why the reduced inflammation is bad. The reduced growth is also no problem in non-pregnant and non-lactating adults. Modern people might be growing too fast, given historical trends. A book I've been reading argues that women used to hit puberty - menarche - at 17 years old, back in the 1800s. But now they hit puberty as early as 12 in countries like the United States. PUFAs are clearly involved in all of this. Maybe "reduced growth" is desirable, even in pregnant/nursing women and children.)
MNHD also notes accumulation of Mead Acid (20:3 n-9) in conditions of EFAD. The determination of EFAD is based on the ratio of Mead Acid to Arachidonic Acid (20:4 n-6), also known as the triene:tetraene ratio. "Normal" ratio is defined as below 0.4:1. (Young cartilage is EFA Deficient by this criteria, as many have noted.)
"The exact requirements for EFA in humans is not clearly defined but is apparently very low. The first study of EFAD, in human adults maintained for 6 months on a diet extremely low in fat, did not produce dramatic symptoms." They reckon it would take over 6 months on an EFAD diet to produce a symptom of deficiency. And PUFAs are almost impossible to avoid in trace amounts.
Moving on to Omega-3, "it has been extremely difficult to demonstrate their essentiality in animal studies", and also "levels of C22:6 n-3 [DHA] in brain and retinal PL are extremely stable despite wide variations in diet." In one study, adult rats fed a fat-free diet only lost 10-20% of the DHA over their entire life-span.
They claim "n-3 EFAD develops only under extreme dietary conditions...[DHA] is selectively retained by the brain, and depletion of [DHA] is difficult after weaning." Finally, they say: "Multigenerational studies in rats have been needed to produce drastic reductions in brain [DHA] levels."
A key revelation is that 18:1 n-9 (oleic acid) "can replace EFA in the lipids of animals and humans." They note "High dietary levels of C18:1 n-9 suppressed desaturation of EFA such that if dietary concentration of [oleic acid] were 10 times higher than that of C18:2 n-6, triene:tetraene ratios indicating EFAD were observed."
The point of all this is that it seems impossible to "eliminate AA from your cells", as Monty claims to have done. Even on fat-free diets, this simply doesn't happen because the body will conserve them. What you can do is increase the ratio of Mead Acid to AA, and this seems to be controlled by ratios of fatty acids in the diet, overall PUFA intake, ratio of carbs to PUFAs, and other factors. If you wanted to "remove" AA from your cells, you would have to eat a diet containing NO PUFAs or NO FAT whatsoever. If you eat butter, or cheese, or eggs, you will have AA in your cells. |
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