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| | From:  rensielk (Original Message) | Sent: 3/14/2008 3:41 AM |
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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To clarify, having a few AA molecules in your body may be impossible to eliminate, but is irrelevant, just as one or two molecules of anything are irrelevant to the human body. The key is to prevent AA from being used when cells are stressed. I've seen the crucial differences in my body: cuts heal more slowly, and with a rubbery scab (though clotting time appears to be at least as quick), inflammation lasts a short period of time (hours, not days), skin rashes disappear, my keloid lost its redness and began to shrink, my hair doesn't feel itchy if I don't wash it often (I now wash once a week with just water, and my full head of hair never gets "greasy," etc.
Also, studies done on native Greenlanders (on an omega 3 rich diet) had much longer clotting times than Danes, who certainly eat their share of fish from northern waters. In any case, if anyone wants to take me up on my offer, we will have me tested for fatty acids, and if I'm classified in the "EFAD" range, you pay. If not, I will pay. Let's get the negotiations started. |
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I'm sure you have a lot less AA in your cells and more Mead Acid than normal people eating high-PUFA oils. But you are moving the goal-posts. You said you had "eliminated"AA in your cells. I agree that you will most likely show up as EFAD, based on the triene:tetraene (Mead:AA) ratio. But that does not mean you have no AA. You might have more AA in your cells than Mead Acid and still be deemed EFAD. I think that criteria for EFAD is flawed, any way.
I've noticed similar benefits from restricting PUFAs. My cuts stop bleeding faster and form a soft scab with no itchiness or inflammation. I noticed years ago while using flax oil that it suppressed my immune system. I got sick easily when I was exposed to cold. I just wash my hair with water, run my hands through it, and comb it gently.
There are some ways that I think we could deplete AA, such as subjecting ourselves to mild stresses. Example: periodic fasting, cold showers, hot-and-cold (contrast) showers, sleep deprivation, high-intensity exercise, ketosis, etc.
What about the argument that people are "growing too fast" nowadays because of PUFAs and junk fats? This book I am reading cites a study (Tanner JM. 1973. Trend toward earlier menarche in London, Oslo, Copenhagen, the Netherlands and Hungary. Nature 243: 75-76). Norway and Finland both had female menarche around 16.5-17.0 years old, back in the early to mid-1800s. By 1970, they were both down near 13 years. They were probably eating a lot of dairy back then and now they are eating PUFAs and junk fats.
Their consumption of sugar and refined carbs was probably less in the 1800s than it is today, going by the trends in other industrialized countries. These two factors combined would accelerate lipid peroxidation, vitamin E depletion, and all of the chronic inflammatory disease we see today. |
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In my family, height and dietary PUFA consumption appear to be very well correlated, and the age of puberty seems to support this as well. It's so obvious to me at this point that it's rather boring. I guess I could get "excited" again if there were some good experiments being conducted, but at this point we can only rely on the evidence that now exists. In England there was a lot of refined sugar consumption in the 1800s, and I agree that it is not opitmal, but it now usually goes hand in hand with a PUFA-rich diet and also a diet deficient in at least some vitamins and minerals, so one would have to control for many factors.
As to "moving the goalposts," I don't agree, and the reason is that in biology and biochemistry, what matters are thresholds - there are few if any absolutes. Almost all the time, a large man will need to drink a lot more alcohol to become intoxicated as compared to a small woman, for example. I don't think there is any physiologically or biochemically relevant amounts of AA anywhere in my body at this point, if there is any at all. One molecule of AA therre might be somewhere. I'm more than willing to discuss a possible experiments about this, with the "loser" to pay for all expenses. |
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