The Science
What Is The Chronic Inflammation Test?
Chronic inflammation is the result of a series of complex cellular reactions. The thromboxane A2 pathway plays a major role in the development and progression of chronic inflammation. Urinary 11-Dehydro Thromboxane B2 (Chronic Inflammation Test) is an indirect measure of thromboxane production. Two of the major components governing the thromboxane A2 pathway are arachidonic acid and Nuclear Factor kappa B.
Arachidonic Acid (Omega-6)
Arachidonic acid, an Omega-6 fatty acid, is a key metabolic source for inflammation. Arachidonic acid is a saturated fat found in many foods, but is also produced from the transformation of other fatty acids by metabolism. How is arachidonic acid produced?
Fatty acids in the diet, such as linolenic acid, transform in the body to the gamma-linolenic acid (GLA) by the action of a cellular enzyme delta-6-desaturase. GLA rapidly converts to dihomo-gamma-linolenic acid (DGLA). DGLA produces many desirable eicosanoids with strong anti-inflammatory effects; however, DGLA is also the substrate for the delta-5-desaturase enzyme that produces arachidonic acid.
Arachidonic acid is converted by both platelet cyclooxygenase-1 (COX-1) and the inflammatory enzyme cyclooxygenase-2 (COX-2) into the powerful eicosanoid, thromboxane A2. Thromboxane A2 makes platelets sticky, leading to blood clots, and causes blood vessels to constrict, raising blood pressure. Thromboxane A2 rapidly converts in the blood to inactive thromboxane B2, which is metabolized by the liver to 11-Dehydro Thromboxane B2 (Chronic Inflammation Test) and is filtered by the kidneys into the urine.
See the effects of nutrition on chronic inflammation and the role of arachidonic acid.
Nuclear Factor kappa B (NFkB)
The NFkB transcription factor is located in an inactive form in the cytoplasm of our cells for the purpose of regulating immune and inflammatory responses. NFkB is a protein that functions as a switch to turn inflammation on and off in our bodies. An important role of NFkB is to induce and maintain the inflammatory state underlying metabolic and chronic diseases, including maintaining the balance of energy governing glycolysis and respiration.
NFkB is definitely one of the most important regulators of the pro-inflammatory expression of genes. NFkB is activated at inflammatory sites in many diseases where it is capable of inducing transcription of pro-inflammatory adhesion molecules, cytokines, chemokines, nitric oxide, and cyclooxygenase-2.
Cyclooxygenase-2 is the enzyme responsible for the formation of thromboxane A2 from arachidonic acid.
During the aging process, the expression of NFkB increases in our body, encouraging systemic chronic inflammation and turning on the genes for chronic diseases we have inherited. Scientists estimate more than 90 percent of chronic diseases are the direct result of chronic inflammation.
See the effects of environmental and external factors on chronic inflammation and the role of NFkB.