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03-10-2016, 03:59 PM | #20 | ||
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However, a few points..... 1. Degree of specific affinity of any lectin for any tissue can vary with patient genetics, as can the propensity for autoimmune reaction. 2. The propensity of the small intestine to allow lectins such as WGA into the bloodstream, ie defeat of "tight junctions", is itself strongly influenced by lectins like WGA. WGA can act as its own vehicle for entering the bloodstream. There are symptoms besides cartilage destruction which accompany arthritis. They include skin rash and swelling of the lower legs. These symptoms are less associated with the more-heat-sensitive WGA, but are more associated with less-heat-sensitive lectins like bean concavalin A and potato lectin. Yes, cartilage destruction is preceded by inflammation. The inflammation is part of the autoimmune process. Inflammation-associated cytokines, usually led by TNF alpha, collect around the lectin attack. Leucocytes follow, and attack the compromised tissue. I could not fail to notice that you challenged me to prove my case without providing any evidence for your case besides your internet-claimed background. Yes, I'm more than willing to concede that doctors and nurses get trained with the information you are attempting to impart. It's just wrong. Suppose that the truth is uncertain? Why would you pipe up to say not to try eliminating lectins? "First, do no harm" does not mean, as medical practitioners tend to say "Instead, remove the patient's knee". http://www.krispin.com/lectin.html |
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"Thanks for this!" says: | caroline2 (03-10-2016) |
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