How do we Manifest Inflammatory Conditions?
- By:Maureen Fontaine
Inflammatory Conditions
Trauma, Catabolism and Disease
When oxygen is utilized by the body, it produces an extremely reactive �exhaust� that is damaging to the cells. The reactive molecules in this exhaust are generally referred to as reactive oxygen species (ROS) or �free radicals�. Whereas some free radicals take part in a required function in the metabolic process. An overload of them is thought by most researchers to be a most important cause of cell destruction, degenerative disease, inflammation, as well as aging.
Among the diseases 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 disorders.
Larger cell production of free radical activity (known as ROS) is linked to nearly all degenerative disorders including heart disease, cancer, arthritis, liver disease, periodontal disease, cataracts, diabetes, macular degeneration, autoimmunity, gastrointestinal diseases, and asthma.
Free radical movement acts in response with (to) cells creating chain reactions that result in tissue damage causing spasms, tenderness, swelling, and disease.
Antioxidants, such as alpha lipoic acid, Coenzyme Q10, anti-catabolic enzymes, NADH (nicotinamide adenine dinucleotide) and such as superoxide dismutase, glutathione peroxidase, and catalase decrease the harm due to (from) free radicals. Younger strong cells generate larger quantities of protective and defensive materials.
Aging and disease cause reduced cell production of defensive compounds leading to amplified damage to cell membranes; unavoidably, destruction to membranes decreases cellular capacity to restore damaged tissue.
Membrane and extra-cellular matrix damage develops into diminished 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) diminishes and shorter chain GAG�s increase, as a result dehydration of tissue takes place 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 preservation.
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) resulting in failure of cell/tissue function.
Consequences:
This results in increased tendency for the following:
� Bruising
� Excessive swelling
� Spasm
� Joint inflexibility
� Digestive abnormalities
� Respiratory distress
Note: Insulin acts as a major transporter to distribute amino acids, glucose, hormones, fatty acids, vitamins and additional elements into the cell so that the cell can create indespensible elements required for tissue repair.
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