More than 20 million Americans are afflicted with the most common type of arthritis, which is called osteoarthritis (OA). OA results from the deterioration of the cartilage in the joints. OA often starts between ages 40-60 and is common in overweight people. In a study published in the October 2003 Obesity Research Journal, Dr. Fountain observed that only 12% of those who were thin had OA joint pain compared to 60% of those who were overweight.

The aging of the baby boomers, coupled with America’s expanding waistlines, makes it likely that millions more Americans will develop OA in the next decade.  Surgery Doesn’t HelpAt the start of the 21st century, physicians were doing 650,000 arthroscopic surgeries each year. The surgeons believed they could reduce knee pain and improve joint motility in patients with OA. Unfortunately, a controlled clinical trial comparing the effectiveness of these arthroscopic procedures to a sham (pretend) operation demonstrated that these surgical procedures worked no better than the “placebo” surgery.1 What Promotes Osteoarthritis?Trauma to the joint can lead to inflammation and more osteoarthritic damage. However, OA appears to be due in part to a chronic low level of inflammation in the joints, which contributes to the breakdown of cartilage even in the absence of severe joint trauma. Elevated levels of CRP (an inflammatory protein) are seen particularly in those with more serious OA.2 Drugs like aspirin, Advil and other nonsteroidal anti-inflammatory drugs (NSAIDS) often reduce the pain and stiffness of osteoarthritic joints within a few days, but taking these drugs for a long time can often irritate the stomach and occasionally cause life-threatening stomach bleeding. The newer NSAIDS (COX-2 inhibitors) can increase blood pressure in those on certain blood pressure medications. Weight Loss HelpsIt has been known for a long time that people who put a lot of weight around their waist are far more likely to end up with osteoarthritic joints. Increased body fat increases the release of certain substances (leptin, cytokines, CRP) in the blood that may play a role in developing OA. A recent study at the Florida Pritikin Center found a 45% drop in CRP levels in older women in just two weeks with proper diet and exercise.3 Glucosamine May Help Repair JointsOne of the molecules the human body uses to make new cartilage and the fluid that lubricates the joints is called glucosamine. However, as people grow older, the production of this natural component of cartilage may not be adequate. Two long-term clinical trials have shown that 1,500 mg/day of glucosamine sulfate prevented the loss of cartilage in osteoarthritic joints and significantly reduced the pain associated with OA.4, 5 The National Institute of Health is currently funding a large clinical trial involving 1,600 people age 40 and older to determine the effectiveness of supplemental glucosamine in slowing or possibly even reversing some of the damage caused to joints by aging, trauma, and inflammation. Methylsulfonylmethane (MSM) is another supplement that has shown promise in reducing OA pain. A recent study found that the combination of glucosamine plus MSM worked better than glucosamine alone to relieve OA symptoms. Vitamin C May Promote OsteoarthritisFor many years, people have been led to believe high doses of vitamin C may protect their joints from OA. Guinea pigs, like humans, require vitamin C in their diet and also develop OA in old age. Vitamin C deficiency can impair cartilage formation and higher doses were believed to help protect joints by blocking free radicals that can damage cartilage. However, a recent study of guinea pigs at Duke University published in the June 2004 Arthritis and Rheumatism journal cast serious doubt on the long-term benefit of high-dose vitamin C supplements for staving off OA. The results showed that high doses of vitamin C did slow the loss of cartilage in the joints over time; but it also stimulated the overproduction of bone growth factor and led to the formation of bony spurs in the joints, which significantly increased joint damage and OA. By James Kenney, PhD, RD, LD, FACNReferences:1. N Engl J Med 2002;34781-82. J Rheuamatol. 1995;22:1527-313. Metabolism 2004;53:377-814. Lancet 2001;357:251-65. Arch Intern Med 2002;163:2113-23