Post
by ofonorow » Sun May 14, 2006 10:58 am
Thanks again, Owen. Just went back to Pauling\'s old book......haven\'t touched it for ages.....and actually found the reference. So ascorbic acid = L-ascorbic acid. Interesting that of the 4 isomers only one is anti-scurvy, so synthetic Vit C must undergo a 75% purifying process. I was possibly thinking of Vit E, which in its synthetic form is a 50/50 mixture of D- and L- forms. Back to the Arctic Diet. Interesting that there are sources of Vit C even on a predominantly meat diet. The double-digit gram doses some of you guys are on is daunting, and one must wonder how you keep it up...especially using diarrhea as the signpost! And our loss of the ability to produce Vit C must be regarded as a deleterious mutation, as there is no natural way of compensating through our food. If the Eskimos indicate anything, is it that you may drastically reduce your Vit C requirement by altering your diet to say exclude carbohydrates? That your \"optimal\" Vit C dose really indicates a suboptimal/unnatural diet? This can surely be easily verified by say going on one of those low-carb diets like Atkins?')
Furthermore, a high saturated fat diet (of the Eskimos) actually reduces levels of Lp(a). So if the Eskimos had better arteries and less Lp(a), how does this impact the Pauling/Rath theory?^M
Yes, I am familiar with autopsy studies. At least two of them have shown that the native Eskimos had less atherosclerosis than nonnative Alaskans:^M
Furthermore, a high saturated fat diet (of the Eskimos) actually reduces levels of Lp(a). So if the Eskimos had better arteries and less Lp(a), how does this impact the Pauling/Rath theory?^M
Two is better than nothing, and notice \"less\", but not zero atherosclerosis. The further information we are getting in the forum provides evidence that the Eskimo diet contains plenty of vitamin C. The Unified Theory predicts higher serum Lp(a) levels at low vitamin C intakes, but not necessarily atherosclerosis. Atherosclerosis is a healing process where the Lp(a) sticks to pieces of lysine and proline that appear after a \"crack\" or lesion in the artery. Slightly elevated Lp(a) shouldn\'t cause atherosclerosis in healthy arteries.
In the context of the eskimo diet, I had questioned whether a low carb diet could greatly spare Vit C, seeing that sugars compete with its entry into cells. If as our Accountant says excluding sugar RAISED his bowel tolerance, that would be the opposite of sparing Vit C, no? Presumably then a high carb diet would LOWER the Vit C bowel tolerance dose because the Vit C would be unable to access cells and tend to spill out into the gut earlier. This seems to call into question the meaning of the bowel tolerance test. It is commonly viewed as a kind of loading test, with the excreted substance regarded as being surplus to requirement, no?^M
The posts on the Eskimo thread are interesting. You wrote:^M
[quote:c4f673600c=\"ofonorow\"]Plaques form out of Lp(a) attracted to the Lysine Binding sites. The plaques serve a purpose. They strengthen collagen starved arteries. My guess is that Eskimos have silent atherosclerosis, something like the youngsters autopsied during the Korean war. ^M
Is anyone familiar with autopsies conducted on Eskimos?^M
Yes, I am familiar with autopsy studies. At least two of them have shown that the native Eskimos had less atherosclerosis than nonnative Alaskans:^M
Furthermore, a high saturated fat diet (of the Eskimos) actually reduces levels of Lp(a). So if the Eskimos had better arteries and less Lp(a), how does this impact the Pauling/Rath theory?^M
Yes, I am familiar with autopsy studies. At least two of them have shown that the native Eskimos had less atherosclerosis than nonnative Alaskans:^M
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Owen R. Fonorow
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