Quote:
Originally Posted by kiwi33
Veggienft, I am puzzled by your post.
RA is an autoimmune disease with a strong inflammatory component - that is why anti-inflammatory agents are often effective in management of it.
Lectins are proteins which bind oligosaccharides with high specificity - each lectin has a different specificity. Exogenous lectins (mainly found in plant foods) can have local effects in the GI tract if the plant food has not been adequately cooked. If the food has been cooked exogenous lectins will not have local effects and (in just the same way as any other protein) will be broken down into their amino acids by digestive enzymes. I don't know of any evidence that intact exogenous lectins can pass across the gut mucosal boundary and enter the blood stream, where they (potentially) might interact with immune system proteins - do you have evidence which suggests that this is the case?
There are also endogenous lectins, naturally made in the human body. Mannan-binding lectin is an example - it, and others, play important roles in the innate immune system.
"The old medical saw which says autoimmune diseases happen when the immune system attacks "self" tissue by mistaking it for "not-self" antigens is simply false."
This statement will come as a considerable surprise to people (like me) whose professional knowledge includes immunology.
Would you like to justify it, ideally with referenced data?
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Different lectins have different heat tolerances, "cooking" can mean many things concerning time, temperature, moisture, and the promulgation of heat to all molecules. Wheat germ agglutinin (WGA) is the lectin in wheat. WGA has a specific affinity for cartilage molecules, the tissue destroyed in rheumatoid arthritis. Glucosamine works to relieve arthritis because glucosamine contains the same molecule-end which cartilage uses to attract WGA. Glucosamine binds WGA which would otherwise be bound by cartilage.
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