Author Topic: Cordain Newsletter  (Read 1818 times)

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Offline TylerDurden

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Cordain Newsletter
« on: February 15, 2010, 06:06:48 pm »
 Lectins and Autoimmune Disease

Rheumatoid Arthritis (RA) is a disease in which the body’s own immune system begins to recognize bone, cartilage, and tissues which serve as a cushion between bones in joints as foreign bodies and will begin to systematically destroy or degrade these tissues. This leads to extreme pain, inflammation, stiffness, and eventual immobility of certain joints. Though the cause of RA is still largely unknown, it has long been known that RA symptoms are highly correlated with inflammation of gut. In this review of RA published in 2000, Dr. Cordain offered some interesting theories of how specific dietary elements may be contributing to both an inflamed gut and RA symptoms.

Gut inflammation is known to increase intestinal permeability, so that the gut becomes less capable of limiting the substances that cross the gut barrier and into the blood stream. Interestingly, 67% of all RA sufferers also suffer from gut inflammation. In this article Dr. Cordain suggested that specific substances known as dietary lectins may be involved in both the inflammation of the gut and in facilitating the movement of bacteria from the gut into the blood stream.

Specific dietary lectins, found in wheat, grains, and legumes, have been shown in animal models to damage intestinal cell walls, leading to an inflamed state. This inflammatory state allows passage of bacteria and other foreign proteins into the blood stream that simply should not be allowed there. Additionally, dietary lectins have been shown to facilitate the preferential growth of specific gut bacteria often associated with RA symptoms. These bacteria share a sequence of proteins very similar to many of our own body’s protein sequences. Immune cells ‘read’ the protein sequences on the bacteria and may begin to associate similar self-proteins with these foreign substances, thus attacking both the bacteria and our own tissues.

Lectins themselves have been shown to be capable of crossing a damaged gut membrane and entering into the bloodstream in tact. It is not known whether dietary lectins bind to synovial tissues in joints. However, in animal models when lectins were injected directly into joints the result was a massive immune response followed by the destruction of joint tissue. If lectins are indeed binding to synovial tissues, this coupled movement of gut bacteria into the blood and lectins' own ability to cause an immune response may be large factors influencing RA symptoms.

Knowing as we do that inflammatory guts and RA are strongly correlated and that dietary lectins are potential causers of inflamed guts it is to our benefit to examine further the connection between the two events and the dietary mechanisms through which these events may be triggered.

Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Brit J Nutr 2000, 83:207-217.
Link to paper.

Lectin-based Food Poisoning

In The Dietary Cure for Acne Dr. Cordain discusses how lectins can inhibit the activity of certain zinc dependent enzymes necessary for the proper breakdown and ‘sloughing off’ of skin cells; a process known as exocytosis. Now research done by the Medical College of Georgia has shown that specific lectins are toxic to certain intestinal cells and can even cause cell death. Similar to the acne story, the lectins present on damaged intestinal cells were shown to prevent the normal process of exocytosis of certain mucus cells needed to keep intestinal cells healthy.

Gastro-intestinal (GI) epithelial cells are constantly exposed to mechanical damage within our stomach and intestines. Fortunately, they have a rapid repair mechanism which typically seals the damaged cell with mucus within seconds to prevent any unwanted food-stuffs from entering our blood stream. However, lectins may be delaying or completely inhibiting this repair process. This is theorized to be the cause some of the GI discomfort experienced with ingestion of beans, or wheat germ agglutinin in those with celiac disease.

Scientists at the Medical College of Georgia introduced a variety of lectins to cultured rat’s gastrointestinal (GI) epithelial cells to examine lectins' potential for binding these cells. Wheat Germ Agglutinin was found to bind most readily. Next scientists created ruptures in the GI epithelial cells using both a laser and a syringe needle to mimic the natural process of cell damage seen during digestion of solid foods. Once damaged, scientists determined the ability of the cells to repair themselves by observing the influx of a dye present in the solution that will not pass through an intact epithelial cell. The GI epithelial cells coated with Wheat Germ Agglutin were incapable of healing and dye leaked through the damage site without restraint.

You can imagine if this were an actual stomach cell within the body being incapable of repairing itself and the subsequent ‘leaking’ of stomach and intestinal contents directly into the bloodstream.

Scientists went on to investigate lectins’ potential for inhibiting the secretion of mucus necessary for GI epithelial cell repair. A culture of mucus secreting GI tract and colon cells were bathed in Wheat Germ Agglutinin and then damaged. Dramatic decreases in mucus secretion (mucus necessary for healing) were observed in concurrence with abnormally large amounts of cellular death in the area surrounding the damage site. The scientists then concluded that lectins are potent inhibitors of mucus secretion in GI epithelial cells and are toxic and even deadly to damaged GI epithelial cells with the likely mechanism being an interruption in exocytosis of mucus from mucus secreting GI and colon cells.

Miyake K, Tanaka T, McNeil PL. Lectin-based food poisoning: a new mechanism of protein toxicity. PLoS ONE. 2007 Aug 1;2(1):e687.
Link to paper.

Diet and Acne

A recently performed dietary intervention published in the Journal of American Academy of Dermatology has examined whether one of two particular diets prescribed to participants was to be more effective than another at decreasing the severity of acne symptoms in the participants.

The intervention recruited 43 male subjects between the ages 15 and 25, all with mild to moderate acne symptoms. Subjects were assigned randomly to either a high Glycemic-load (HGL) diet or a low Glycemic-load (LGL) diet. Details of subjects' height, weight, body fat percentage, body mass index, and, most importantly, their visible acne lesion count, were collected at 0, 4, 8, and 12-weeks on their prescribed diet. Also investigated were the accompanying changes, if any, observed in subjects’ fasting levels of insulin, blood glucose, and other markers correlated with acne severity.

Subjects within the LGL experimental group were educated about the Glycemic index and on how to replace high Glycemic-index foods with foods containing higher protein content and with lower Glycemic-indices (meats, whole grains, and fruits). The control HGL group was not educated about the Glycemic index and was instructed to include carbohydrates regularly as a part of their diet. Compliance was strictly monitored using several control mechanisms.

After twelve weeks the results of the intervention were apparent to investigators. The LGL dieters experienced a significantly greater reduction in acne lesion count than did the HGL diet counterparts. In addition, LGL dieters improved their weight, body fat percentages, and waist circumferences significantly. Also of interest were the changes observed in the LGL dieters’ insulin sensitivity levels and how it directly correlated with their decreased acne lesion counts, indicating a relationship between insulin sensitivity and acne severity.

Smith, R.N., Mann, N.J., Braue, A., Makelainen, H., Varigos, G.A., The effect of a high-protein, low Glycemic-load diet versus a conventional, high Glycemic-load diet on biochemical parameters associated with acne vulgaris: A randomized, investigator-masked, controlled trial. Journal of American Academy of Dermatology 2007; 57:247- 256.
Link to paper.
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