More than 52 million Americans suffer from some form of arthritis.1
Conventional medical wisdom has long held that rheumatoid arthritis results from an autoimmune attack on joints, while osteoarthritis was thought to result from age-related “wear-and-tear.”
For the first time, a team of researchers2 at Stanford University has demonstrated that this is not true!
It turns out that osteoarthritis is accompanied by the same pathological, pro-inflammatory immune factors involved in rheumatoid arthritis. Even more compelling was their finding that, if treatment is initiated before symptoms manifest, osteoarthritis may be entirely prevented.
Unfortunately, the list of available drugs to combat autoimmune disorders—including long-term treatment with corticosteroids likeprednisone—is notoriously limited and comes with life-threatening complications, including obesity and diabetes.
The exciting news is a novel intervention has been identified that safely regulates the immune system to protect aging joint tissue from autoimmune attacks.
In this article, you will learn about UC-II®, a form of undenatured type II collagen. Its unique molecular characteristics prevent immune cells’ overreaction to proteins normally found in cartilage and joint tissue that lead to pain and stiffness in both rheumatoid andosteoarthritis.3-7
In multiple clinical trials using this proprietary collagen formulation, scientists at Harvard8 have been able to achieve relief of arthritic symptoms, with some patients experiencing complete remission!9
You will also learn how UC-II®’s mode of action may be synergistically enhanced when combined with Boswellia serrata and two other joint-renewing nutrients.
The Stanford team’s discovery of the autoimmune link between osteoarthritis and rheumatoid arthritis was first presented in late 2011.
A group of 25 scientists concluded that the development of osteoarthritis is in great part driven by low-grade inflammatory processes.2,10 Specifically, the researchers discovered that the body launches an orchestrated, powerful attack on the synovial joints via signaling proteins normally used to fight infections. This autoimmune response, they reported, plays a key role in osteoarthritis onset.2
Synovial joints are the most common joint types in the human body. They contain soft-tissue cushioning in addition to cartilage, along with synovial fluid, a natural lubricant. Knees, hips, and shoulders are just a few of the commonly arthritic joints that fall into this category.
What the Stanford team found was that low-grade inflammation is not merely an early symptom of osteoarthritic cartilage destruction in synovial joints—it is the trigger that causes it. The study also revealed that by targeting the autoimmune derangements that occur early on in the development of osteoarthritis, arthritis might be completely preventable.
They went on to point out that drugs intended to inhibit the arthritic reaction (like corticosteroids) paradoxically compromise the immune system.2 It would be far safer, they reported, if a natural way to turn off the body’s abnormal response were available.