Why we Attain Inflammatory Conditions.
Inflammatory Conditions
Trauma, Catabolism and Disease
When oxygen is used by the body, it produces an very reactive �exhaust� that is damaging to the cells. The reactive molecules in this exhaust are often referred to as reactive oxygen species (ROS) or �free radicals�. While some free radicals take part in a mandatory function in the metabolic process. An overload of them is considered by many researchers to be a most chief cause of cell obliteration, degenerative disease, inflammation, as well as aging.
Among the disorders attributed to enlarged free radical action are arthritis, digestive diseases, heart disease, liver disease, diabetes, cancers, cataracts, macular degeneration (age-related vision loss), auto-immune disease and breathing conditions.
Larger cell production of free radical activity (known as ROS) is connected to nearly all degenerative conditions including heart disease, cancer, arthritis, liver disease, periodontal disease, cataracts, diabetes, macular degeneration, autoimmunity, gastrointestinal diseases, and asthma.
Free radical activity acts in response with (to) cells creating chain reactions that result in tissue damage creating spasms, tenderness, inflammation, and degeneration.
Antioxidants, such as alpha lipoic acid, Coenzyme Q10, anti-catabolic enzymes, NADH (nicotinamide adenine dinucleotide) and such as superoxide dismutase, glutathione peroxidase, and catalase reduce the harm due to (from) free radicals. Younger strong cells produce larger amounts of protective and defensive materials.
Aging and disease cause reduced cell development of protective compounds leading to amplified damage to cell membranes; consequently, harm to membranes reduces cellular capacity to restore damaged tissue.
Membrane and extra-cellular matrix harm creates weakened ideal first-intention healing concerning parenchyma (the tissue of an organ).
Cell damage leads to Inflammation:
Dehydration Results in Failure of Cell Function
As production of long chain glycosaminoglycans (GAG�s) lessens and shorter chain GAG�s increase, as a result dehydration of tissue transpires and resulting in failure of membrane function.
Membrane Receptivity to Growth Factors is Lost
Injury desensitizes cell membrane to growth factors (insulin, somatomedins, etc.) necessary for cell communication, repair, defense, and maintenance.
Break down of Tissue
Deposits of greatly glycosylated, inflexible and compacted collagen types V and VI increase.
Poor Ability to Heal
Increased granulomatous (term associated to nodular inflammatory lesions), second intention healing involving stromal elements (progress of scar tissue) resultant in loss of cell/tissue function.
Consequences:
This results in increased tendency for the following:
� Bruising
� Extreme inflammation
� Spasm
� Joint rigidity
� Digestive disorders
� Respiratory distress
Note: Insulin acts as a primary transporter to distribute amino acids, glucose, hormones, fatty acids, vitamins and additional elements into the cell so that the cell can create necessary elements required for tissue repair.
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