Issue link: https://cp.revolio.com/i/571399
Page 28| Abby's Magazine - www.AbbysMag.com Advanced glycation end products (AGEs) also promote inflammation. While AGEs are formed in our bodies, especially when blood sugar is frequently elevated, they can also be absorbed from the diet. A diet high in pre-formed AGEs can seriously elevate blood levels of various inflammatory mediators, including C-reactive protein, tumor necrosis factor-alpha, and vascular cell adhesion molecule. A low-AGE diet can lower these inflammatory bio-chemicals. What promotes the formation of AGEs in food? High heat/prolonged cooking. Deep-fried foods, such as French fries, fried fish and shrimp, fried chicken, etc. are great sources of AGEs. Well-done meats (including typical fast-food burgers), overly-crisp bacon, burnt toast, indeed anything cooked with high heat or for prolonged periods provides an AGE-rich diet. The Vegetable Oil Connection A major contributor to chronic inflammation in modern America is the widespread use of vegetable oils, especially corn, safflower, soy, peanut, cottonseed, sunflower and canola oils. These oils are rich in the omega-6 fatty acid linoleic acid. In the body, linoleic acid is converted to arachidonic acid. Arachidonic acid is the raw material from which the body makes a broad range of proinflammatory biochemicals. When arachidonic acid is processed by cyclooxygenase enzymes, inflammatory prostaglandins and thromboxanes are produced. When arachidonic acid is processed by lipoxygenase enzymes, inflammatory leukotrienes are produced. Vegetable oils are a recent addition to the human diet. They only came into widespread industrial production in the 1920s. Over the past 40 years, as the anti- cholesterol medical/dietary establishment has told Americans to reduce their saturated fat intake, it has hyped the intake of linoleic acid-rich vegetable oils. The common use of vegetable oils has caused a historically unprecedented shift in the diet-induced inflammatory balance. Linoleic acid is a powerful inducer of a proinflammatory micro-environment in the cells that line our arteries and veins. Not only does high linoleic acid intake promote elevated levels of inflammatory prostaglandins, thromboxanes and leukotrienes, but it also activates other powerful inflammatory molecules, including tumor necrosis factor-alpha (which in turn activates the superinflammatory interleukin-6) and nuclear factor kappa Beta. Nuclear factor kappa Beta in turn has the power to turn on the genes that promote production of over seven other proinflammatory cytokines and biochemicals. Omega-3s and the Modern American Diet The dietary counterbalance to linoleic acid/arachidonic acid is provided by the omega-3 fatty acids, alpha-linolenic acid and the fish oil fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA at adequate blood/cellular levels can reduce conversion of linoleic acid to arachidonic acid, and reduce the conversion of arachidonic acid to inflammatory prostaglandins, thromboxanes and leukotrienes. Omega-3 fatty acids also don't have the strong proinflammatory effect that linoleic acid does. Before the widespread use of vegetable oils, it is generally estimated that the dietary omega-6-to- omega-3 ratio was around one or two to one, so there was a good dietary anti-inflammatory counterbalance. In the vegetable oil-rich typical American diet of the past 40 years, the omega-6-to-omega-3 dietary ratio tends to be 20 to one or more! This is due both to a reduction of dietary levels of omega-3 fatty acids, as well as an increase of omega-6 fatty acids. Thus the severely imbalanced fatty acid profile of the typical modern American diet has profoundly shifted our cellular biology to a proinflammatory status. Obesity and Inflammation A majority of the American population is now considered overweight or obese. Recent research has established that obesity is a major contributor to the chronic inflammatory state. According to researchers Lee and Pratley, "Obesity is characterized by a chronic, systemic low-grade state of inflammation. Biomarkers of inflammation, such as the leukocyte [white blood cell] count, tumor necrosis factor-alpha (TNF-