Rheumatoid Arthritis – when your body declare war on itself !




As opposed to Osteoarthritis which is caused by wearing and tearing down cartilage in joints through a lifetime of use, Rheumatoid Arthritis is caused by an autoimmune response that causes the immune system to attack it’s own body.

There’s no cure and there’s no way of healing it since there’s no blood flow to the cartilage. if diagnosed early then Rheumatoid Arthritis can however be stoped or slowed down from progressing. However only 50% of treated patients will experience a reduction in disease activity. Since Rheumatoid Arthritis also carries and increased risk of cardio vascular diseases that number is way to low.

in the latest article I looked at Omega 3 as a natural way of reducing or even eliminate the pain from Arthritis – However a study published last year in JCI insight takes it a step further.

Because Omega 3 is a precursor to the prostaglandin ( a group of compounds with hormone like effect) group Specialized Proresolving Lipid Mediators (SPM) that decreases inflammation and inhibits the neutrophils that attacks the joints, these scientists decided to see if fish oil suppelements could raise SPM levels in patients with Rheumatoid Arthritis.

The trial did show an increase of the SPM Resolvin, along with significantly reduced joint inflammation to keep it short – the study more then implied that Rheumatoid Arthritis can be stoped by the use of a potent Omega 3 supplement.

Furthermore a study published in Annals of The Rheumatic Diseases on people who are genetically at risk of Rheumatoid Arthritis actually showed that fish oil plays a huge role in preventing rheumatoid Arthritis by regulating the number of antibodies that cause the disease.

These studies along with the knowledge we have on Omega 3 and pain relief makes it a must to be taking fishtail if you have Rheumatoid Arthritis.

Further Rading and source material:

Proresolving and cartilage-protective actions of resolvin D1 in inflammatory arthritis

Omega-3 fatty acids are associated with a lower prevalence of autoantibodies in shared epitope-positive subjects at risk for rheumatoid arthritis