KappArest 180 caps Biotics Research
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A proprietary formula designed to downregulate inflammatory pathways, primarily through the inhibition of NF-kappaB, a molecule inside each cell.
4 capsules 1-3 times per day or as directed by a healthcare provider
Introduction to NF-KappaB
As a ubiquitous nuclear transcription factor that promotes the activation of genes that encode for inflammatory mediators and enzymes, NF-kappaB can be thought of as the major intracellular “amplifier” which ultimately increases the production of the direct mediators of inflammation such as cytokines, prostaglandins, leukotrienes, nitric oxide and other reactive oxygen species (“free radicals”). The process of inflammation begins when two subunit proteins—p50 and p65—merge in the cytoplasm to form NF-kappaB, which is kept in an inactive state by inhibitor kappaB (IkB). When triggered by "negative" stimuli such as traumatic injury, IkB is phosphorylated and destroyed by inhibitor kappaB kinase (IKK). The destruction of IkB allows NF-kappaB to move into the nucleus of the cell where it binds with DNA and activates genes encoding for inflammatory responses. These genes then elaborate their inflammatory products such as interleukin-1 (IL-1), IL-6, tumor necrosis factor, and the proinflammatory destructive enzymes including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), the lipoxygenases (LIPOX), and the matrix metalloproteinases (MMP) including collagenase and gelatinase, which degrade connective tissue. Nitric oxide synthase catalyses the formation of nitric oxide (NO-), which plays an important role in the development of peripheral osteoarthritis6 and spinal disc degeneration7 via oxidative destruction of articular tissues. Cyclooxygenase transforms arachidonic acid into prostaglandins and thromboxanes, which recruit leukocytes to the area of inflammation, exacerbate edema, sensitize peripheral neurons to increased pain perception, and ultimately facilitate the liberation of proteinases, such as matrix metalloproteinases, which destroy joint structures. Present in several isoforms, the lipoxygenase enzyme acts on arachidonic acid to produce leukotrienes that also increase inflammation, joint destruction, and production of MMP. Overall, this same inflammatory response contributes to the genesis and perpetuation of numerous conditions associated with inflammation.