[soho]

Hi Shawna

Here are two segments I found from a paper entitled “Do dietary lectins cause disease?”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115436/

The first segment talks about the mechanisms by which lectins cause diabetes.

The second segment explains why everyone who eats lectins does not develop diabetes.

I also found some papers that postulate that lectins may cause insulin resistance.

My point is that I agree that lectins may be an evil force to be reckoned with. It is just that there are many many arguments supporting both sides of the do lectins cause this or that and in who or how many debate and there is know way we can bring this to closure in this forum.

What I do know through my experience with about 50 dogs who had diabetes is that once a dog has diabetes the clock starts ticking and unless the guardian of that dog makes a heroic effort to control that dogs blood sugar the devastation begins! I also know that the amount of carbohydrates that a dog consumes is directly related to rate of devastation.

Injected insulins are most effective at matching the curve of glucose metabolism when used in small amounts. Injected insulins can be plotted along a graph where one axis is time and the other axis is amount of insulin. In order to closely mimic the graph of carbohydrate absorption with the graph of insulin absorption small amounts of each must be used. As you increase the amount of carbs consumed it becomes more and more impossible to match with the use of injected insulin. Therefore the total amount of carbohydrate consumed is the most important factor in controlling diabetes and avoiding the devastation that this disease usually causes

First segment of paper:
Of particular interest is the implication for autoimmune diseases. Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells.9 The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetyl lactosamine,10 which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together—a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice.11 Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.

Second segment of paper:
But if we all eat lectins, why don’t we all get insulin dependent diabetes, rheumatoid arthritis, IgA nephropathy, and peptic ulcers? Partly because of biological variation in the glycoconjugates that coat our cells and partly because these are protected behind a fine screen of sialic acid molecules, attached to the glycoprotein tips.10 We should be safe. But the sialic acid molecules can be stripped off by the enzyme neuraminidase, present in several micro-organisms such as influenzaviruses and streptococci. This may explain why diabetes and rheumatoid arthritis tend to occur as sequelae of infections. This facilitation of lectins by micro-organisms throws a new light on postinfectious diseases and makes the folklore cure of fasting during a fever seem sensible.