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Inflammation, Pain, and Chronic Disease: An Integrative Approach To Treatment and Prevention

Tanya Edwards, MD, MEd

Abstract
During the past decade, we have begun to develop a clearer understanding of the pathogenesis of many diseases that are associated with aging. Most diseases that carry the largest burden in terms of morbidity and mortality in our culture have their underlying etiology in the inflammatory process.1 Inflammation has been characteristically described as redness, swelling, pain, and heat, potentially leading to the loss of function. We now have a clearer understanding of the mediators that are involved in the inflammatory process. The most commonly defined mediators associated with this process of inflammation are the n-6 eicosanoids, prostaglandin E2, leukotriene B4, as well as the cytokines interleukin-1-ß (IL-1-ß) and tumor necrosis factor- a (TNF-a).2 These mediators are derived predominately from activated leukocytes that migrate into the target area as part of the inflammatory process. There is currently much interest in the literature regarding methods to allay this inflammatory process, including pharmacological anti-inflammatory drugs, as well as dietary manipulations, which aim to improve the balance between pro-inflammatory and anti-inflammatory foods.

Oxidative stress leads to apoptotic injury, which involves early loss of cellular membrane asymmetry, as well as the eventual destruction of genomic DNA. Oxidative stress occurs when oxygen free radicals are generated in excess through the reduction of oxygen. Reactive oxygen species (ROS) include oxygen free radicals and associated entities, which include superoxide free radicals, hydrogen peroxide, and singlet oxygen. Many of these species are produced at low levels during normal physiologic conditions, and they are scavenged by endogenous antioxidant systems that include superoxide dismutase, glutathione peroxidase, catalase,

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