CONDITIONS OF USE: The information in this database is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is safe, appropriate or effective for you or anyone else. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment.
Omega-3 fatty acids have been shown to disrupt inflammation cell signaling pathways by binding to the GPR120 receptor.  This benefit however can be inhibited or even reversed if the ratio of Omega-6 / Omega-3 is too high as Omega-6 serves as a precursor to inflammatory chemicals ( prostaglandin and leukotriene eicosanoids ) in the body.   A high proportion of omega-6 to omega-3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.  Omega-6 competes with Omega-3 for the same rate limiting factor which is required for the health-benefits of Omega-3, directly reducing the action of Omega-3 in addition to pharmacologically counteracting Omega-3 benefits through its own action as a pro-inflammatory agent.
NSAIDs may reduce the benefit of drugs used for treating hypertension because NSAIDs may increase blood pressure. NSAIDs decrease the elimination of lithium ( Eskalith ) and methotrexate ( Rheumatrex ) potentially leading to their toxicity, and reduce the action of diuretics ("water pills") by reducing blood flow to the kidneys. NSAIDs increase bleeding by decreasing the activity of blood platelets and therefore formation of blood clots. When used with other drugs that also increase bleeding, for example, warfarin ( Coumadin ), the likelihood of bleeding complications is increased. Prolonged use of NSAIDs with drugs that increase bleeding should be avoided.