“Chronic low-grade inflammation is now considered to be a critical pathological factor underlying many modern chronic diseases, including diabetes, cardiovascular disease, cancer, and neurodegenerative diseases, and is associated with aging. Chronic low-grade inflammation is characterized by elevated circulating levels of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, and IL-6. A primary cause Read More →

  Abbreviations: ATIs: amylase and trypsin enzyme inhibitors HFD: high-fat diet HPA axis: hypothalamic-pituitary-adrenal axis IAP: intestinal alkaline phosphatase (aka alkaline phosphatase) IL1-β: interleukin 1 beta LPSs: lipopolysaccharides NF-kB: nuclear factor kappa B PUFAs: polyunsaturated fatty acids TLRs: toll-like receptors TLR4: toll-like receptor 4 TNF-α: tumor necrosis factor alpha WGA: wheat germ agglutinin Today I Read More →

Colon Anatomy

  This is a short post about an intriguing study done in rodents to assess what effect different polyunsaturated fatty acids (PUFAs) have on progression of ulcerative colitis (UC). (1) Ulcerative colitis is defined by Taber’s medical dictionary as: “An inflammatory bowel disease marked pathologically by continuous inflammation of the intestinal mucosa, which typically involves Read More →

  “Saturated fats are benign with regard to inflammatory effects, as are the MUFAs [monounsaturated fats]. The meager effect that saturated fats have on serum cholesterol levels when modest but adequate amounts of polyunsaturated oils are included in the diet, and the lack of any clear evidence that saturated fats are promoting any of the Read More →

  Today I want to continue my discussion of foods, drinks and drugs that tend to aggravate an infected and inflamed gastrointestinal mucosa. Fiber The last post covered gut bacteria’s well-known ability to produce intestinal gas by fermenting fiber. However, dietary fiber, especially insoluble fiber, has other damaging characteristics. As I’ve mentioned before, fiber swells Read More →

    In this post, I discussed how unlikely it is that normal digestion of long-chain fatty acids is the source of the pathogens initiating arterial plaque formation. If anything, I showed how protective chylomicrons are in preventing just that. This then leaves us with increased intestinal permeability as the most likely source of translocating Read More →