As a medical professional, I see and treat many different types of arthritis everyday. However, when athletes talk about arthritis, it is osteoarthritis (OA) or degenerative joint disease (DJD) they are concerned about. OA is the oldest and most common type of arthritis. It is characterized by the breakdown of a joint’s cartilage. Cartilage is the material that lines the joints and the ends of the bones. Cartilage breakdown causes the bones to rub against each other. When this happens, the result is pain, stiffness and loss of movement within the affected joint.
OA is a process that occurs over time, most commonly affecting middle-aged to older people. The symptoms can range from very mild to very severe. OA can involve any joint but generally is found in the hands, weight-bearing joints and the spine. Women are more commonly affected than men. Current estimates are that over 20 million Americans have OA. Eighty percent of these people reported that their symptoms have caused a decreased quality of life.
What causes OA? Does exercise contribute to the risk of getting OA, or does it help protect against OA? What can we do to prevent OA? These are questions fitness professionals should be ready to answer.
Medical professionals define OA as either primary OA or secondary OA. Primary OA is the normal breakdown of cartilage that occurs over time without any other known cause. Secondary OA is the development of OA as a result of traumatic injury or as a result of overuse of a joint. Certain occupations put people at a higher risk of OA, and certain sports put individuals at a higher risk of secondary OA.
What causes primary OA? There are two factors that stand out: time and weight. There is a genetic component in OA that makes some individual’s symptoms more severe than others. But the fact is, as we age, OA develops simply because we erode more joint cartilage than the body replaces. The other strong link to OA is excess weight. Individuals who are overweight during or after the age of 45 have a significantly higher rate of OA, especially in the knees.
What causes secondary OA? Again, there are two main factors: injury and repetitive use.
Here is where fitness professionals need to know the latest research. Exercise can cause OA in people who develop joint injuries as a result of their training or activity. What these injuries have in common is that they set up inflammation in the affected joint. Inflammation can lead to damage to the cartilage, which can then lead to OA. This scenario defines secondary OA because it happens secondarily to a process other than aging.
Secondary OA may occur in people who are relatively young and may affect joints not normally involved in OA, such as a carpenter developing OA in an elbow. However, the most commonly affected joints are the hips and knees.
Certain sports are more associated with secondary OA than others. Running and weight-bearing exercises are the most likely to put the participant at a higher risk. That’s because highly repetitive, stressful exercising like running tends to wear down the protective cartilage in the joint more quickly than normal wear and tear. Some studies suggest that certain people who already have slight abnormalities in their joints and their joint alignment make up the large majority of individuals susceptible to this process.
Does exercise contribute to the risk of getting OA, or does it help protect us against it? The answer is both! The vast number of middle-aged and older individuals with primary OA need exercise to reduce the impact of OA on their lives. Regular exercise is essential to this group to maintain their ideal body weights. Moderate exercise is also essential to build strong muscles to support the joints and increase both endurance and flexibility.
The individuals who participate in activities that wear down protective cartilage need to listen to their bodies. The symptoms of joint swelling and pain after vigorous exercise indicate a marked risk of secondary OA that should not be ignored or covered up with medication. This is where fitness professionals can influence clients to make the right choices.
What can we do to prevent OA? The fact is, if we live long enough, there is very little we can do to prevent OA. A more important issue is, can we do anything to minimize the impact of OA on our lives? Obviously, as has been said before, maintaining a normal body weight is an effective prevention strategy. A diet rich in long-chained omega-3 free fatty acids, EPA and DHA and antioxidant rich fresh fruits and vegetables also helps by reducing inflammatory responses within the body. The other thing we can do is to help the body maintain healthy protective cartilage as long as possible.
Normal joint cartilage contains two key molecules: glucosamine sulfate and chondroitin sulfate. Glucosamine sulfate is a form of amino sugar that stimulates cartilage formation. Chondroitin sulfate is part of a large protein molecule (proteoglycan) that gives cartilage elasticity. The body makes both these compounds. They do not come from food we eat.
Researchers found that glucosamine sulfate and chondroitin sulfate can be safely taken as a supplement. Glucosamine is extracted from crab, lobster and shrimp shells. Chondroitin is extracted from either shark or bovine cartilage. The shark cartilage is a better choice because it eliminates the risk of Mad Cow Disease.
The medical establishment really became interested in these molecules after the publication of the first long-term study of 212 patients in 1999. Glucosamine halted the progression of structural joint damage and reduced symptoms among patients with knee OA in a placebo-controlled trial lasting three years. The group of individuals who took 1,500 mg of glucosamine experienced no significant joint space narrowing after three years. Joint space narrowing is the main radiological marker of joint damage. The placebo group experienced joint space narrowing that was consistent with the normal progression of OA when left untreated. Since 1999, there have been several more studies that have confirmed the ability of glucosamine, and even better results when chondroitin sulfate was taken together, to halt joint damage progression.
What does this mean? The research has provided significant data that the body recognizes glucosamine sulfate and chondroitin sulfate when taken as a supplement and uses these molecules to maintain healthy protective cartilage. Safety and side effect profiles have shown no evidence that glucosamine sulfate or chondroitin sulfate cause harm. The result is we now have a solution for those individuals who are at risk for secondary OA. We also have a strategy for individuals who want to delay the impact of primary OA on their active lifestyles as long as possible.
Fitness professionals have a need to know about OA and about the emergence of alternative treatments like glucosamine sulfate and chondroitin sulfate. I hope this article has provided you the basic information necessary to provide the best advice possible to your clients.
- TE McAlindon et al. Glucosamine and chondroitin for treatment of osteoarthritis. JAMA 2000 283: 1469-1473.
- JY Reginster et al. Long-term effects of glucosamine sulfate on osteoarthritis progression: a randomized, placebo-controlled clinical trial. Lancet 2001 352: 253-256.
- Institute for Clinical Systems Improvement (ICSI). Diagnosis and treatment of adult degenerative joint disease. May 2002 p 42-59