Gout is a chronic degenerative disease which means

You do not "catch" Gout ... it is a deterioration of cartilage that covers the ends of the bones.

Gout is a common type or arthrisis. Gout occurs when crystals of uric acid invade the joints. The major cause of Gout is hyperuricaemia, high levels of uric acid in the blood. Uric acid is a normal component of your body but becomes toxic when serum levels rise above six milligrams per 100 milliliters, by the time the levels rise to seven milligrams per 100 milliliters, sharp crystals start forming in joints, tendons, kidneys, and other tissues, where they cause excruciating pain, especially to joints rich in nerves, such as the big toe.

Some of the first symptoms of gout is intense pain, usually only in one joint. The first joint of the big toe is common in nearly half of the first attacks, and at some point in over ninety percent of individuals with gout. If the attack progress fever and chill will appear. The first attacks usally occur at night caused by a event, such as

If we examine data collected from the earliest lesions to the most advanced stages of clinical Gout, the process contributing to Gout appears to be able to be stopped and, in many cases, reversed. [J.H. Bland and S. M. Cooper,"Gout : A Review of the Cell Biology Involved and Evidence for Reversibility: Management Rationally Related to Kown Genesis and Pathophysilolgy," Seminars on Arthritis and Rheumatism 14 (1984): Pgs 106-133. The major therapeutic goal appears to be enhancing repair of the collagen matrix and regeneration by the connective-tissue cells.]

Some of the side effects of aspirin and nonsteroidal anti-inflammatory drugs (NASIDs)--such as ibuprofen (Motrin, Nupron, Advil), piroxicam (Feldene), diclofenac (Voltaren),fenoprofen (Nalfon), indomethacin (Indocin), naproxen (Naprosyn),tolmetin (Tolectin), and sulindac (Clinoril)-- are well-known: gastrointestinal upset, ulcer formation, headaches, dizziness, etc. A less well-known side effect is further degeneration of the joint cartilage. Experimental studies have shown that NSAID use is associated with aceleration of oeteoarthritis and increased joint destruction[P.M. Brooks, S.R. Potter and W.W. Buchanan,"NSAID and Gout-- Help or Hindrance," J Rheutatol 9 (19820: 3-5. N.M.Newman, R.S.M. Ling, "acetabular Bone Destruction Related to Non-Steroidal Anti-inflmatory Drugs," Lancet 2 (1985):11-13]

While Gout affects individual joints, rheumatoid arthritis affects all of the body's synovial joints. Joints afflicted with rheumatoid arthritis tend to make a sound like crinkling cellophane, whereas osteoarthritic joins make popping, clicking, and banging noises.

The spondyloarthropathies are a group of rheumatic disorders that tend to affect the spine. Ankylosing Spondylitis (AS) is the most common of these. In this disorder, certain joints of the spine become inflamed, stiffen, become rigid, and then fuse together. If confined to the lower back, AS causes virtually no limitation of movement. In some cases, however, the entire spine may become rigid and bent. If the joints between the ribs and spine are affected, breathing problems may result as the chest wall's ability to expand becomes limited.

The onset of rheumatoid arthritis is often associated with physical or emotional stress; however, poor nutrition or bacterial infection may also be involved. Rheumatologists have discovered that the blood of many people with RA contains antibodies called rheumatoid factors, a finding that can aid in early diagnosis of the condition.

Also food allergies and abnormal bowel function (i.e. leaky gut) may combine and result in the increased circulation of gut-derived antigens into other areas of the body. The body produces antibody-antigen complexes (immune complexes) characteristic of RA to battle these gut-derived foreign antigens; but these antibody-antigens are thought to also cross-react with antigens in the joint tissues. In other words, the antibodies formed to attack the (leaky gut) microbes also cross-react and attack joint collagen.
[A. Ebringer, et al. "Klebsiella Antibodies in Ankylosing Spondylitis and Proteus Antibodies in Rheumatoid Arthritis." Britain Journal of Rheumatology v.25 (1986) p.2772-2785]

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