Plant Poisons and Rotten Stuff – The Blog

Everything makes more sense with the leukotriene connection, for example, the fact that a wide spectrum of autoimmune diseases are connected with food chemical intolerance.

One of the conversation points that is grossly overshadowed by the very tiresome “it’s sat fat and cholesterol/it’s not sat fat and cholesterol” heart disease debate, is the fact that there is actually quite a lot of evidence to suggest that heart disease is an autoimmune disease; that like a number of autoimmune diseases it is associated with chronic inflammation, and high leukotriene levels.

There are 224 citations in pubmed for leukotrienes + heart disease. Included are a paper demonstrating that a gene variation in FLAP that increases leukotriene production doubles the risk of heart attacks. FLAP polymorphisms have also been highlighted in asthma. Read a brief discussion here. And a paper with an amusingly puzzled abstract regarding “aspirin insensitive eicosanoid biosynthesis in cardiovascular disease” which points out the now rather obvious fact that “enhanced production of vasoactive cysteinyl leukotrienes (cys-LTs) occurs in unstable angina despite conventional antithrombotic and antianginal treatment.” Which they would, wouldn’t they, because salicylates cause that to happen, not prevent it as the authors were hoping.

The involvement of salicylates in leukotriene production would account for that rash of contradictory studies over recent years that show that aspirin and other NSAIDs thin the blood but somehow increase the likelihood of stroke and heart attack. The fact that particular genes are associated with enhanced leukotriene production and salicylate intolerance in asthma makes me feel as though I’ve uncovered a sneaky mass-extermination experiment that involves killing off genetically salicylate intolerant individuals with a baby aspirin prescription.