By Joel Fuhrman, M.D. www.drfuhrman.com
Understanding And Preventing Our Nation’s Primary Crippler!
Osteoarthritis (OA) is a nearly universal degenerative condition, affecting both men and women as they age. OA is the most common type of arthritis, affecting more than 28 million adults in the United States.
In OA, the cartilage cushion in the joints breaks down, which eventually can cause the bones to rub together. Pain, stiffness, and sometimes the formation of bone growths, called spurs, result. OA can affect any joint, but it is most common in the hands, feet, spine, and in large, weight-bearing joints such as the hips and knees. OA of the hip and knee represents the leading cause of pain and disability in adults in the U.S. OA is often referred to as the “primary crippler” of adults, and the percentage of the population with these symptoms has been increasing in recent years.1
OA also is called degenerative joint disease (DJD) or ordinary arthritis. It differs from rheumatoid arthritis (RA) as it does not involve an immune system-mediated attack on the joints as is the case with RA.
Despite its prevalence and the fact that it worsens with age, OA is not the inevitable consequence of aging. Recent scientific advances have enabled us to better understand the contributory factors that promote arthritis, dispelling the myth that joint degeneration is merely an age-related phenomenon.
Currently, the pathogenesis of OA is explained by various contributing factors that adversely affect cartilage cells. In simple terms, the chondrocytes (cells that produce cartilage) become stressed, overworked, injured, and eventually die. This destruction of the chondrocytes makes it impossible for your body to keep up with the production of high-quality collagen needed for normal wear and tear. As the cartilage erodes, the joint becomes inflamed, and lytic (caustic) enzymes can further degrade the cartilage matrix. As cartilage wears away on the ends of the bones and cushioning is lost, the intensity of pain may increase. Pain may become quite severe if the cartilage has completely deteriorated.
Surprisingly, physical inactivity can be more harmful to the joints than overuse. Joint activity signals for the delivery of nutrients to the joints. A lack of exercise or varied movement can weaken the muscles that support the joints, and an underused joint may become stiff, painful, dysfunctional, and prone to injury and osteoarthritis.
Joints, because of their somewhat unusual blood supply, are extremely sensitive to negative nutritional influences compared with other parts of the body. When we abuse our body with poor nutrition, we not only raise our blood pressure and increase our risk of heart attack and stroke, but we also damage our joints. In fact, OA and degenerative bone disease of the spine could be early warning signs of heart disease in years to come.
The reason why joints have an increased susceptibility to damage from dietary folly is because of their indirect blood supply. Instead of direct oxygenation and nourishment from being bathed in blood (such as with muscles and organs), cartilage is nourished from the fluid in the joint capsule. Oxygen comes from tiny capillaries that surround the joint capsule and diffuses across the joint capsule membrane and into the joint fluid. With normal microcirculation and good nutrition, plenty of oxygen and nutrients bathe the cartilaginous surface of the joints.
This intricate and fragile system can be vulnerable to nutritional stresses. The nourishment to the cartilaginous surface of the joint can be curtailed even by the smallest impediment to normal blood flow. When atherosclerosis is present, the delivery system can be easily disrupted by as simple a thing as eating a high-fat meal. Even the earlier stages of atherosclerosis can impede oxygen delivery to the joint, revealing itself in joint problems that occur decades before the heart problem is diagnosed.
When you eat a piece of high-fat food—such as cheese pizza, bacon, or steak—the saturated fats thicken the blood and make the red blood cells sticky. This clumping together of red blood cells makes them too large to enter the small capillaries that surround and nourish the joint capsules. Atherosclerotic deposits thicken the walls and narrow the vascular bed, further impeding delivery of oxygen and nutrients to the joint area where most cartilage and bone remodeling takes place. Defective remodeling then occurs, with gradual destruction of the joint.
High Nutrient Supply
High cholesterol levels and other blood markers of heightened cardiovascular risk are a documented risk factor for both knee and generalized osteoarthritis.2 It is not difficult to understand why osteoarthritis is related to meat and cheese consumption, since sufferers of both conditions are more likely to have high cholesterol and high triglyceride levels. These are typical signs of a diet that promotes atherosclerosis, impaired circulation, and subsequent cartilage compromise.3
Populations with lower rates of heart disease, such as the Chinese, correspondingly have lower rates of osteoarthritis in the same age bracket. The elderly in Beijing, China were found to have 80-90 percent less osteoarthritis than elderly Americans.4 Radiographic signs of arthritis in the age range of 60-89 were found in only about one percent in the Chinese portion of the study, and the percentage did not increase with age.
Cardiac risk factors also are risk factors for arthritis, but there is more to the story. Marginal nutrient intake also can interfere with the chondrocytes’ ability to make structurally strong cartilage. Contrary to the view held for many years, in osteoarthritis the cartilage does not passively erode away; in fact, the body works hard to protect itself. In the early years when the joints are stressed by improper nutrition, the body increases the production of cartilage in an attempt to compensate. The production of cartilage matrix has been observed to increase as much as six times the normal amount in the beginning phase of osteoarthritis.
The problem lies in the production of poor quality cartilage. Without optimal nutrition, DNA synthesis goes on, but does not perform singing the best tune. As time goes on and the disease advances, the chondrocytes start to die and collagen synthesis falls.
Mounting research has pointed to the fact that a high intake of carotenoids, particularly lutein and beta-cryptoxanthin, found in colorful vegetables, is necessary for high quality cartilage.5 Studies also have shown that low levels of boron, selenium, glutathione, and sulfur are related to osteoarthritis incidence and exacerbation.6 The good news is that if osteoarthritis is caught early—before much loss of cartilage and death of chondrocytes—and nutritional excellence is initiated, most of the damage still can be reversible.
Fish oil supplements, docosahexaenoic acid (DHA), glucosamine, and chondroitin have been shown to be helpful in retarding the advancement and reducing the symptoms of osteoarthritis.7 Eicosapentaenoic acid (EPA) and DHA have anti-inflammatory properties that can reduce joint inflammation, and glucosamine and chondroitin can supply nutrients needed for cartilage synthesis. Keep in mind, however, that just as with other diseases, supplements alone are not all that is necessary for optimal results. However helpful supplements may be, without the adoption of a superior diet containing the full concert of healthful phytochemicals and antioxidants that results in low cholesterol, one cannot expect maximum healing and maximum protection against OA. Once excellent nutrition is instituted, the body adequately produces its own cartilage precursors, and supplements have little effect.
1. Christmas C, Crespo CJ, Franckowiak SC, et al. How common is hip pain among older adults? Results from the third National Health and Nutrition examination survey. J Fam Prac 2002;51(4):345-8.
2. Cheras PA, Whitaker AN, Blackwell EA, et al. Hypercoagulability and hypofibrinolysis in primary osteoarthritis. Clin Orthop 1997;334:57-67. Al- Arfaj AS. Radiographic osteoarthritis and serum cholesterol. Saudi Med J 2003;24(7):745-7.
3. Cheras PA, Whitaker AN, Blackwell EA, Sinton TJ, et al. Hypercoagulability and hypofibrinolysis in primary osteoarthritis. Clin Orthop 1997:334:57-58.
4. Nevitt MC, Xu L, Zhang Y, et al. Very low prevalence of hip osteoarthritis among Chinese elderly in Beijing, China, compared with whites in the United States: the Beijing osteoarthritis study. Arthritis Rheum 2002;46(7):1773-9.
5. De Roos AJ, Arab L, Renner JB, et al. Serum carotenoids and radiographic knee osteoarthritis: the Johnston County Osteoarthritis Project. Public Health Nutr 2001;4(5):935-42.
6. Devirian TA, Volpe SL. Dietary vitamins and selenium diminish the development of mechanically induced osteoarthritis and increase the expression of antioxidative enzymes in the knee joint of STR/1N mice. Crit Rev Food Sci Nutr 2003;43(2):219-31.
7. McAlindon TE, LaValley MP, Gulin JP, Felson DT. Glucosamine and Chondroitin for Treatment of Osteoarthritis: A Systematic Quality Assessment and Meta-analysis. JAMA 2000;283:1469-1475. Towheed TE, Anastassiades TP, Shea B, et al. Glucosamine therapy for treating osteoarthritis. Evidence-Based Nursing 2001;4:121 or Cochrane Database Syst Rev 2001;(1): CD002946 (latest version 8 Dec 1999).